1 00:00:01,000 --> 00:00:04,000 Good morning, class. Nice to see you here, 2 00:00:04,000 --> 00:00:08,000 you loyal holdouts, the stalwarts who haven't gone home early for 3 00:00:08,000 --> 00:00:12,000 Thanksgiving. You recall that last time we were talking about the 4 00:00:12,000 --> 00:00:16,000 Matevoidic system, and much of the rationale for 5 00:00:16,000 --> 00:00:20,000 studying it stems from two reasons. First of all, it recapitulates in a 6 00:00:20,000 --> 00:00:25,000 formal sense what happens during embryogenesis, 7 00:00:25,000 --> 00:00:29,000 i.e. one has relatively undifferentiated stem cells which 8 00:00:29,000 --> 00:00:33,000 are able to differentiate into a number of different directions by 9 00:00:33,000 --> 00:00:37,000 committing themselves to either the myeloid or lymphoid compartment, 10 00:00:37,000 --> 00:00:41,000 and then going down yet other pathways, more detailed pathways to 11 00:00:41,000 --> 00:00:46,000 generate a whole variety of cell types. 12 00:00:46,000 --> 00:00:50,000 Secondly, we really understand the differentiation pathways of 13 00:00:50,000 --> 00:00:54,000 Matevoisis better than we understand any tissue in the body, 14 00:00:54,000 --> 00:00:59,000 in no small part because it's much easier to study the soluble cells in 15 00:00:59,000 --> 00:01:03,000 the blood and in the immune system than it is to study how these 16 00:01:03,000 --> 00:01:08,000 processes happen in normal tissues. But having said that, 17 00:01:08,000 --> 00:01:13,000 I want to emphasize the fact that in each of our tissues there are 18 00:01:13,000 --> 00:01:18,000 oligopotential stem cells. When I say oligopotential I mean 19 00:01:18,000 --> 00:01:24,000 they can go down several different pathways. Recall up there on that 20 00:01:24,000 --> 00:01:29,000 diagram we talked about pluripotential which means multiple, 21 00:01:29,000 --> 00:01:34,000 and today we're going to talk a bit about todipotential stem cells, 22 00:01:34,000 --> 00:01:39,000 which are able to disperse descendants into all the different 23 00:01:39,000 --> 00:01:45,000 differentiation lineages in the body. 24 00:01:45,000 --> 00:01:50,000 At the end of our last lecture, we were focusing on the red blood 25 00:01:50,000 --> 00:01:56,000 cells. And this is sometimes called erythropoiesis, 26 00:01:56,000 --> 00:02:02,000 which is to say the process by which red blood cells are generated. 27 00:02:02,000 --> 00:02:06,000 We mentioned the concept of homeostasis, and homeostasis just 28 00:02:06,000 --> 00:02:11,000 refers to the fact that all of these systems are in very delicate balance 29 00:02:11,000 --> 00:02:15,000 so that the body can respond to the physiologic needs of the organism at 30 00:02:15,000 --> 00:02:20,000 any one point in time. We talked about the fact that for 31 00:02:20,000 --> 00:02:24,000 example when there's a massive infection in the body, 32 00:02:24,000 --> 00:02:29,000 then the homeostatic mechanisms allow an increase in these kinds of 33 00:02:29,000 --> 00:02:34,000 immune cells in order to encounter the infection. 34 00:02:34,000 --> 00:02:38,000 And at the end of our last lecture, we were talking about this specific 35 00:02:38,000 --> 00:02:43,000 branch, and how in fact homeostasis is maintained there. 36 00:02:43,000 --> 00:02:48,000 And what we see here is a series of committed progenitors. 37 00:02:48,000 --> 00:02:52,000 So when I talk about committed progenitors I'm referring to cells 38 00:02:52,000 --> 00:02:57,000 that have already made the commitment to go down one 39 00:02:57,000 --> 00:03:02,000 or another pathway. They're not yet fully differentiated. 40 00:03:02,000 --> 00:03:06,000 As you can see here, we have first forming cells and 41 00:03:06,000 --> 00:03:10,000 colony forming cells. We don't need to remember all the 42 00:03:10,000 --> 00:03:14,000 different abbreviations except to say that these cells here are in a 43 00:03:14,000 --> 00:03:18,000 relative undifferentiated state. And the only end stage 44 00:03:18,000 --> 00:03:22,000 differentiation comes at the very end here when we get to red blood 45 00:03:22,000 --> 00:03:26,000 cells. We said in general that it's the case that most highly 46 00:03:26,000 --> 00:03:30,000 differentiated cells are post-mitotic, which is to say 47 00:03:30,000 --> 00:03:34,000 they're never going to reenter into the growth and division cycle of the 48 00:03:34,000 --> 00:03:38,000 cell that we talked about earlier in the semester. 49 00:03:38,000 --> 00:03:42,000 And that's obviously dictated here by the fact that this erythrocyte 50 00:03:42,000 --> 00:03:46,000 lacks a nucleus, i.e. during the final stage of 51 00:03:46,000 --> 00:03:50,000 differentiation, in addition to accumulating large 52 00:03:50,000 --> 00:03:54,000 amounts of hemoglobin in its cytoplasm, this cell actually pops 53 00:03:54,000 --> 00:03:58,000 out its nucleus, and that obviously represents an 54 00:03:58,000 --> 00:04:02,000 irrevocable change in that cell can never again enter into growth 55 00:04:02,000 --> 00:04:06,000 and division cycle. The immediate precursor of an 56 00:04:06,000 --> 00:04:12,000 erythrocyte is often called an erythroblast. And the term blast 57 00:04:12,000 --> 00:04:17,000 here refers to a cell of embryonic appearance. Blast is used often to 58 00:04:17,000 --> 00:04:23,000 indicate, we'll mention that again shortly, a cell which looks very 59 00:04:23,000 --> 00:04:28,000 primitive, and embryonic, and undifferentiated. And that ends 60 00:04:28,000 --> 00:04:34,000 up going into an erythrocyte, which we said is actually a synonym 61 00:04:34,000 --> 00:04:40,000 for a red blood cell, an RBC, a red blood cell. 62 00:04:40,000 --> 00:04:44,000 And we talked about the fact that this progression is actually 63 00:04:44,000 --> 00:04:49,000 maintained and furthered by the stimulus of the compound called 64 00:04:49,000 --> 00:04:53,000 erythropoietin. So, we're using some of the same 65 00:04:53,000 --> 00:04:58,000 words over and over again. And erythropoietin is essentially a 66 00:04:58,000 --> 00:05:03,000 growth factor which stimulates the end stage differentiation of the 67 00:05:03,000 --> 00:05:08,000 erythroblast into the erythrocyte. 68 00:05:08,000 --> 00:05:13,000 Epo, as erythropoietin's often abbreviated, is actually made in the 69 00:05:13,000 --> 00:05:19,000 kidneys. And it's made in the kidneys in response to the 70 00:05:19,000 --> 00:05:25,000 physiological stimulus of hypoxia. Hypoxia means inadequate 71 00:05:25,000 --> 00:05:31,000 oxygenation of the tissues. You might ask, well, why is red 72 00:05:31,000 --> 00:05:37,000 blood cell contractions controlled, as they are, in the kidney? 73 00:05:37,000 --> 00:05:41,000 And the fact is, we don't really know why evolution 74 00:05:41,000 --> 00:05:45,000 has chosen the kidney as the site of monitoring the degree of oxygenation 75 00:05:45,000 --> 00:05:49,000 of the blood. And in response to hypoxia, it begins to crank out 76 00:05:49,000 --> 00:05:53,000 erythropoietin, or Epo. You can think of 77 00:05:53,000 --> 00:05:57,000 erythropoietin as an extracellular liggon just like a growth factor. 78 00:05:57,000 --> 00:06:01,000 It has its own cognate receptor on the surface of the erythroblast, 79 00:06:01,000 --> 00:06:06,000 and when Epo released by the kidney hits an erythroblast in the context 80 00:06:06,000 --> 00:06:11,000 of the bone marrow, it actually has two effects. 81 00:06:11,000 --> 00:06:16,000 It happens to be the case that roughly even 95% of the erythroblast 82 00:06:16,000 --> 00:06:21,000 that are made routinely are forced to go into apitosis under routine 83 00:06:21,000 --> 00:06:26,000 conditions. So, this is an enormously wasteful 84 00:06:26,000 --> 00:06:31,000 system, i.e. as every moment we speak, 90 or 95% of the erythroblast 85 00:06:31,000 --> 00:06:37,000 that have come into existence in your bone marrow apitose. 86 00:06:37,000 --> 00:06:43,000 They never go into end stage differentiation. 87 00:06:43,000 --> 00:06:50,000 But when Epo is around, Epo provides a strong anti-apoptotic 88 00:06:50,000 --> 00:06:56,000 signal to the red blood saves some and maybe even all of the 89 00:06:56,000 --> 00:07:03,000 erythroblasts from their normal fate of undergoing apitosis. 90 00:07:03,000 --> 00:07:07,000 So here, if we imagine there are actually two fates, 91 00:07:07,000 --> 00:07:12,000 one is to become an erythrocyte, and the other is to apitose, where 92 00:07:12,000 --> 00:07:16,000 the aptisosis is paradoxically enough the dominant fate of the cell, 93 00:07:16,000 --> 00:07:21,000 the moment that an Epo comes on the scene, it blocks this alternative 94 00:07:21,000 --> 00:07:25,000 fate, allowing these cells to mature. Epo at the same time stimulates the 95 00:07:25,000 --> 00:07:30,000 erythroblast to differentiate. Now, you might as yourself the 96 00:07:30,000 --> 00:07:35,000 question, why is there this enormously inefficient process? 97 00:07:35,000 --> 00:07:38,000 An enormous effort is made to crank out large, astronomical numbers of 98 00:07:38,000 --> 00:07:42,000 erythroblasts, and yet most of them are wasted even 99 00:07:42,000 --> 00:07:46,000 before they've had a chance to undergo end stage differentiation. 100 00:07:46,000 --> 00:07:50,000 And the rationale here is as follows. This is a terrific system 101 00:07:50,000 --> 00:07:54,000 for rapidly ramping up the level of red blood cells in your circulation 102 00:07:54,000 --> 00:07:58,000 because here, within a matter of a day or two, one can crank up, 103 00:07:58,000 --> 00:08:02,000 actually in a matter of hours, you can crank up the rate of 104 00:08:02,000 --> 00:08:06,000 production of red blood cells by maybe even a factor of ten. 105 00:08:06,000 --> 00:08:10,000 Instead of having 90% of the erythroblast apitose, 106 00:08:10,000 --> 00:08:14,000 let's say 0% of them do so, and therefore, instead of having 10% 107 00:08:14,000 --> 00:08:18,000 of the erythroblasts becoming red blood cells, 100% of them will do so. 108 00:08:18,000 --> 00:08:22,000 And therefore, you have the virtually miraculous 109 00:08:22,000 --> 00:08:26,000 response that if you go from here high up in the rocky mountains at 110 00:08:26,000 --> 00:08:30,000 ten or 12,000 feet, within a matter of two or three days, 111 00:08:30,000 --> 00:08:34,000 your red blood cell concentration actually has compensated, 112 00:08:34,000 --> 00:08:38,000 has risen up to create the oxygen caring capacity that enables you to 113 00:08:38,000 --> 00:08:42,000 deal with the thin oxygen, with the low oxygen tension that's 114 00:08:42,000 --> 00:08:47,000 present at high altitudes. Now, having said that, 115 00:08:47,000 --> 00:08:52,000 the fact is that there is an Epo receptor on the surface of the 116 00:08:52,000 --> 00:08:58,000 erythroblast, and what we see there is the following. 117 00:08:58,000 --> 00:09:01,000 Let's talk about the erythroblast and just blow it up a little bit. 118 00:09:01,000 --> 00:09:05,000 So, here's the erythroblast. That's the undifferentiated 119 00:09:05,000 --> 00:09:08,000 precursor. And by the way, the erythroblast is actually still a 120 00:09:08,000 --> 00:09:12,000 white blood cell. Often we call a white blood cell a 121 00:09:12,000 --> 00:09:15,000 leukocyte. You may know that gluco means white. So, 122 00:09:15,000 --> 00:09:19,000 a leukocyte, it's still white. And after the erythropotent 123 00:09:19,000 --> 00:09:22,000 impinges on it, one of the things it starts doing is 124 00:09:22,000 --> 00:09:26,000 to make the hemoglobin, which turns it into a red blood cell. 125 00:09:26,000 --> 00:09:30,000 At this stage, it's still white. On the surface of the erythroblast 126 00:09:30,000 --> 00:09:35,000 are these Epo receptors. I'll just abbreviate them like this, 127 00:09:35,000 --> 00:09:40,000 Epo receptor, and once it binds the liggon Epo just like the growth 128 00:09:40,000 --> 00:09:45,000 factor receptors, we talked early in the receptors 129 00:09:45,000 --> 00:09:49,000 signals are sent into the erythroblast to stimulate both 130 00:09:49,000 --> 00:09:54,000 differentiation and to prevent the initiation of the cell suicide 131 00:09:54,000 --> 00:09:59,000 program that we call apitosis. Interestingly, one of the things 132 00:09:59,000 --> 00:10:04,000 that happens normally is the following, that when these signals 133 00:10:04,000 --> 00:10:09,000 come in, there is an enzyme called a phosphotase which is attracted 134 00:10:09,000 --> 00:10:14,000 to the receptor. The Epo receptor works like a 135 00:10:14,000 --> 00:10:18,000 tyrosine kinase growth factor receptor that we talked about 136 00:10:18,000 --> 00:10:22,000 earlier in the semester. And here, we have an enzyme, 137 00:10:22,000 --> 00:10:27,000 a phosphotase, which actually counteracts the function of the 138 00:10:27,000 --> 00:10:31,000 tyrosine kinases. So, after the Epo receptor has 139 00:10:31,000 --> 00:10:35,000 bound its liggon, here's the plasma membrane, 140 00:10:35,000 --> 00:10:40,000 it has a whole series of I'll draw Y here for tyrosine. 141 00:10:40,000 --> 00:10:43,000 It has a whole series of phosphates attached to it because of the 142 00:10:43,000 --> 00:10:47,000 actions of tyrosine kinase enzymes that are associated with its 143 00:10:47,000 --> 00:10:51,000 cytoplasmic domain indirect analogy to what we talked about in the case 144 00:10:51,000 --> 00:10:54,000 of growth factor receptors. But, one of the things that happens 145 00:10:54,000 --> 00:10:58,000 is that this phosphotase, which removes phosphates, then gloms 146 00:10:58,000 --> 00:11:02,000 onto the receptor like this. It grabs hold of some of these 147 00:11:02,000 --> 00:11:06,000 tyrosine kinases. And what this phosphotase does is 148 00:11:06,000 --> 00:11:10,000 reach around. It reaches around and it begins to prune off all of these 149 00:11:10,000 --> 00:11:14,000 phosphates because that's what a phosphate does. 150 00:11:14,000 --> 00:11:19,000 It cuts away all the phosphates, thereby directly reversing the 151 00:11:19,000 --> 00:11:23,000 previous actions of the tyrosine kinase that led to the formation of 152 00:11:23,000 --> 00:11:27,000 these phosphates, and that in turn allows downstream 153 00:11:27,000 --> 00:11:32,000 signaling to occur. This is obviously a functional 154 00:11:32,000 --> 00:11:36,000 negative feedback loop, i.e. whenever there is an agonist 155 00:11:36,000 --> 00:11:40,000 you want an antagonist. Whenever there's a stimulus which 156 00:11:40,000 --> 00:11:44,000 is induced in the body, there has to be an inhibitory signal, 157 00:11:44,000 --> 00:11:48,000 and this is part of the whole issue of homeostasis, 158 00:11:48,000 --> 00:11:52,000 the balance between forward and backward. Interestingly enough, 159 00:11:52,000 --> 00:11:56,000 there's a family in Finland, I believe, which has a mutant receptor. 160 00:11:56,000 --> 00:12:01,000 And their mutant receptor lacks this tyrosine. 161 00:12:01,000 --> 00:12:04,000 And what happens as a consequence is that that particular tyrosine 162 00:12:04,000 --> 00:12:07,000 doesn't get phosphorolated. Because that tyrosine doesn't get 163 00:12:07,000 --> 00:12:11,000 phosphorolated, the phosphotase cannot be attracted 164 00:12:11,000 --> 00:12:14,000 to the receptor because there isn't a tyrosine there. 165 00:12:14,000 --> 00:12:18,000 There's some other amino acid residue. I don't know what it is. 166 00:12:18,000 --> 00:12:21,000 It's not important, but it's not a tyrosine. And this cannot happen 167 00:12:21,000 --> 00:12:24,000 because they don't have this tyrosine. This phosphotase could 168 00:12:24,000 --> 00:12:28,000 not be attracted to the receptor to shut it down as it normally 169 00:12:28,000 --> 00:12:32,000 would be. So normally homeostasis is 170 00:12:32,000 --> 00:12:36,000 imbalanced, and several members of this family have become Olympic 171 00:12:36,000 --> 00:12:41,000 cross-country ski winners. They've become Olympic champions. 172 00:12:41,000 --> 00:12:45,000 Why? Because their Epo receptor's hyperactive. Because the Epo 173 00:12:45,000 --> 00:12:49,000 receptor's hyperactive, they have higher than normal levels 174 00:12:49,000 --> 00:12:54,000 of red blood cells in the circulation, and this clearly allows 175 00:12:54,000 --> 00:12:58,000 them to function better in cross country skiing, 176 00:12:58,000 --> 00:13:03,000 which as you know is a really physically demanding task. 177 00:13:03,000 --> 00:13:06,000 Again, I'm not saying this is a good thing for them necessarily. 178 00:13:06,000 --> 00:13:10,000 There are other things in life besides, believe it or not, 179 00:13:10,000 --> 00:13:14,000 winning cross country Olympic competitions because as I mentioned 180 00:13:14,000 --> 00:13:18,000 last time, having too many red blood cells in your circulation, 181 00:13:18,000 --> 00:13:22,000 there's a downside to it which is that you have a much greater 182 00:13:22,000 --> 00:13:26,000 tendency to have occlusions, to have blood clots in your 183 00:13:26,000 --> 00:13:30,000 circulation which obviously is not a very good thing to have. 184 00:13:30,000 --> 00:13:38,000 Oh, so is there a threshold of Epo 185 00:13:38,000 --> 00:13:41,000 receptor activation before phosphotase shuts it down? 186 00:13:41,000 --> 00:13:44,000 These things are not really well understood, are not well studied. 187 00:13:44,000 --> 00:13:47,000 The fact is, you might be able to say we should make a mathematical 188 00:13:47,000 --> 00:13:51,000 model of all of these different circuitry. But the fact is if you 189 00:13:51,000 --> 00:13:54,000 want to make a mathematical model, you have to know some of the 190 00:13:54,000 --> 00:13:57,000 constants. You have to know some of the parameters, the binding 191 00:13:57,000 --> 00:14:00,000 constants. And in fact, for most of the 192 00:14:00,000 --> 00:14:04,000 signaling interactions, no one's ever really studied them in 193 00:14:04,000 --> 00:14:08,000 such great detail. So, one really doesn't know how 194 00:14:08,000 --> 00:14:11,000 much phosphate you need here before the phosphotase becomes really 195 00:14:11,000 --> 00:14:15,000 active. And so, there's not a really good 196 00:14:15,000 --> 00:14:19,000 mathematical model of this feedback loop, even though we know without 197 00:14:19,000 --> 00:14:22,000 any doubt that it exists. So, I want to get into other issues 198 00:14:22,000 --> 00:14:26,000 that are related to the whole issue of accumulated differentiation 199 00:14:26,000 --> 00:14:30,000 traits as one moves down this pathway. 200 00:14:30,000 --> 00:14:34,000 Again, we've used this as a model for how differentiation takes place 201 00:14:34,000 --> 00:14:38,000 in the entire body. The faith that's been implicit in 202 00:14:38,000 --> 00:14:42,000 this kind of scheme for the last 20 or 30 years is that this acquisition 203 00:14:42,000 --> 00:14:47,000 of different kinds of phenotypes is not accompanied by genetic changes, 204 00:14:47,000 --> 00:14:51,000 that is, in the genomes of these cells. I.e. one can accomplish 205 00:14:51,000 --> 00:14:55,000 these different kinds of differentiation not by rearranging 206 00:14:55,000 --> 00:15:00,000 genes but just by rearranging transcriptional programs, 207 00:15:00,000 --> 00:15:03,000 and that the DNA sequence of these cells as they proliferate and 208 00:15:03,000 --> 00:15:07,000 differentiate is fully unchanged. And that's a matter of faith 209 00:15:07,000 --> 00:15:11,000 because you could say to me, how do you know that it's really 210 00:15:11,000 --> 00:15:15,000 true. The fact is that people have looked at genes in many kinds of 211 00:15:15,000 --> 00:15:18,000 cell types, but it's essentially impossible, or it has been at least 212 00:15:18,000 --> 00:15:22,000 until recently, to preclude the possibility that as 213 00:15:22,000 --> 00:15:26,000 cells move down these differentiation pathways, 214 00:15:26,000 --> 00:15:30,000 they begin to change the nucleotide sequences of different 215 00:15:30,000 --> 00:15:33,000 ones of their genes. In fact, I've already told you about 216 00:15:33,000 --> 00:15:37,000 one instance where that's clearly the case. And that is in the 217 00:15:37,000 --> 00:15:41,000 differentiation of the B cells of the immune system, 218 00:15:41,000 --> 00:15:45,000 which happen to be right up here on this chart, because as you recall 219 00:15:45,000 --> 00:15:48,000 from our discussion vis-à-vis immunology, the B cells actually do 220 00:15:48,000 --> 00:15:52,000 rearrange their genes in order to cobble together DNA sequences that 221 00:15:52,000 --> 00:15:56,000 together are able to enable them to make antibodies that are able to 222 00:15:56,000 --> 00:16:00,000 react to specific antigens. So there, there's no doubt at all 223 00:16:00,000 --> 00:16:04,000 that there's a somatic rearrangement of the genes, somatic meaning it's 224 00:16:04,000 --> 00:16:08,000 not a germ line change. It's happening in the soma outside 225 00:16:08,000 --> 00:16:12,000 of the germ line. There's a somatic mutation. 226 00:16:12,000 --> 00:16:16,000 It's not a mutation that's deleterious, but rather is directed 227 00:16:16,000 --> 00:16:20,000 towards a physiologically normal and desirable end point. 228 00:16:20,000 --> 00:16:24,000 But for example, how do you know that when you remember things in the 229 00:16:24,000 --> 00:16:28,000 brain, part of the memory does not derive from changing the DNA 230 00:16:28,000 --> 00:16:32,000 sequence and different neurons in the brain? 231 00:16:32,000 --> 00:16:36,000 What's the molecular basis of memory? Could it be that each time we learn 232 00:16:36,000 --> 00:16:41,000 some things that there are different nucleotide sequences, 233 00:16:41,000 --> 00:16:45,000 critical nucleotide sequences, that are changed in neurons in the 234 00:16:45,000 --> 00:16:50,000 brain, and that those nucleotide sequence changes represent an 235 00:16:50,000 --> 00:16:54,000 important basis for ensuring that memory is retained over decades of 236 00:16:54,000 --> 00:16:59,000 time. Or, rather than having genetic changes in the brain, 237 00:16:59,000 --> 00:17:03,000 might it all be epigenetic, i. . all the other changes that happen 238 00:17:03,000 --> 00:17:08,000 to the cell besides changing DNA sequences in the chromosomal DNA. 239 00:17:08,000 --> 00:17:13,000 So, here we're dealing with the dialectic between epigenetic and 240 00:17:13,000 --> 00:17:19,000 genetic. And, have we talked about DNA methylation 241 00:17:19,000 --> 00:17:24,000 here? Yes, so we talked about DNA methylation, and do you recall or 242 00:17:24,000 --> 00:17:30,000 having discussed the fact that when DNA gets methylated, 243 00:17:30,000 --> 00:17:36,000 that suppresses the transcription of a gene. 244 00:17:36,000 --> 00:17:39,000 But that doesn't change the nucleotide sequence, 245 00:17:39,000 --> 00:17:43,000 and that methylation configuration of a gene can be passed to one cell 246 00:17:43,000 --> 00:17:46,000 generation to the next. It's heritable, but it's not 247 00:17:46,000 --> 00:17:50,000 genetic in the strictest sense of the term, i.e. 248 00:17:50,000 --> 00:17:54,000 it doesn't involve a change in nucleotide sequence, 249 00:17:54,000 --> 00:17:58,000 which is what we want to limit this term to referring. 250 00:17:58,000 --> 00:18:02,000 So, epigenic can represent all the changes in the cell including DNA 251 00:18:02,000 --> 00:18:07,000 methylation, alterations in transcription, 252 00:18:07,000 --> 00:18:12,000 and all other downstream events that result in changes in the cell. 253 00:18:12,000 --> 00:18:17,000 And how can one address this? Well, there are different ways of 254 00:18:17,000 --> 00:18:22,000 addressing this question or addressing the possibility that in 255 00:18:22,000 --> 00:18:27,000 fact there are changes in the nucleotide sequence of the gene. 256 00:18:27,000 --> 00:18:32,000 One way to do this is the following. And that is to take cells from an 257 00:18:32,000 --> 00:18:37,000 early embryo, and here we see an early vertebrate embryo. 258 00:18:37,000 --> 00:18:42,000 This looks really more like a frog embryo or a slightly different shape, 259 00:18:42,000 --> 00:18:47,000 and here we see an early embryo. It's after a blastula. It's called 260 00:18:47,000 --> 00:18:52,000 a blastocyst. Here again we have the word blast. 261 00:18:52,000 --> 00:18:57,000 How about one question per lecture? We have to have some equity here. 262 00:18:57,000 --> 00:19:02,000 Other people can ask questions. It's good to ask questions, 263 00:19:02,000 --> 00:19:06,000 but how about one per lecture; that's fair, equitable. 264 00:19:06,000 --> 00:19:10,000 All right, so here's an early vertebrate embryo. 265 00:19:10,000 --> 00:19:14,000 Here we see the blastocyst. This comes after the earlier stages 266 00:19:14,000 --> 00:19:18,000 in the embryo, and here we see the inner cell mass. 267 00:19:18,000 --> 00:19:22,000 And as it turns out, the inner cell mass is going to be the precursor of 268 00:19:22,000 --> 00:19:26,000 many of the tissues of the ultimately arising embryo. 269 00:19:26,000 --> 00:19:30,000 And here, one can do an interesting experiment. One can take cells out 270 00:19:30,000 --> 00:19:34,000 of the inner cell mass. And one can begin to propagate them 271 00:19:34,000 --> 00:19:38,000 in culture. And what one ends up with is embryonic stem cells. 272 00:19:38,000 --> 00:19:42,000 And the intrinsic interest of embryonic stem cells is manifold. 273 00:19:42,000 --> 00:19:46,000 For one thing, you can take embryonic stem cells and you can 274 00:19:46,000 --> 00:19:51,000 genetically alter them. You can put a new gene in, 275 00:19:51,000 --> 00:19:55,000 in the case of a mouse, or you can take another gene out. 276 00:19:55,000 --> 00:19:59,000 And then what you can do is you can inject the genetically altered 277 00:19:59,000 --> 00:20:04,000 embryonic stem cell into the blastocyst of another embryo. 278 00:20:04,000 --> 00:20:08,000 So let's say we take the cells out of the inner cell mass. 279 00:20:08,000 --> 00:20:13,000 We develop embryonic stem cells. We can call them ES cells. That's 280 00:20:13,000 --> 00:20:17,000 what they're called in the trade, ES cells. We take them out. We can 281 00:20:17,000 --> 00:20:22,000 propagate them in culture. And then, what we can find is we'll 282 00:20:22,000 --> 00:20:26,000 put a genetic marker in those ES cells. Let's say we put in those 283 00:20:26,000 --> 00:20:31,000 embryonic stem cells the marker for the gene beta-galactosidase. 284 00:20:31,000 --> 00:20:35,000 And beta-galactosidase in the presence of a proper indicator, 285 00:20:35,000 --> 00:20:39,000 if you put a proper indicator and make a cell turn blue. 286 00:20:39,000 --> 00:20:43,000 So now we have an ES cell line that produces the beta-galactosidase 287 00:20:43,000 --> 00:20:47,000 enzyme. The beta-galactosidase enzyme beta-gal itself has no effect 288 00:20:47,000 --> 00:20:51,000 on the biology of the cells. It's only a marker. And now, 289 00:20:51,000 --> 00:20:55,000 we take those ES cells, and we inject them into another embryo, 290 00:20:55,000 --> 00:21:00,000 a wild type embryo that lacks this beta-gal marker. 291 00:21:00,000 --> 00:21:05,000 And what we can see is that we inject the ES cells into this 292 00:21:05,000 --> 00:21:10,000 blastocyst. The injected ES cells will now insinuate themselves, 293 00:21:10,000 --> 00:21:15,000 will now intrude into the massive cells in this embryo into which we 294 00:21:15,000 --> 00:21:20,000 injected the ES cells, and they will become part of the 295 00:21:20,000 --> 00:21:25,000 entire embryo genesis that follows. I.e. soon these foreign ES cells 296 00:21:25,000 --> 00:21:30,000 will weasel their way into this inner cell mass. 297 00:21:30,000 --> 00:21:34,000 And they will become established and become functionally equivalent to 298 00:21:34,000 --> 00:21:38,000 the inner cell mass cells that were resident there prior to this 299 00:21:38,000 --> 00:21:42,000 injection. And what you can do then is follow the subsequent fate of, 300 00:21:42,000 --> 00:21:46,000 in this case, a mouse. And what will happen often is that you can 301 00:21:46,000 --> 00:21:50,000 find blue cells all over the mouse sometimes in the paws, 302 00:21:50,000 --> 00:21:54,000 sometimes in the coat. Let's imagine that the hair would turn 303 00:21:54,000 --> 00:21:58,000 blue, which in fact is not the case. But let's imagine the hair would 304 00:21:58,000 --> 00:22:02,000 turn blue. So here's the mouse, 305 00:22:02,000 --> 00:22:06,000 happy because it's part of an important experiment. 306 00:22:06,000 --> 00:22:11,000 And what you'll sometimes see is that, well, remember that art was 307 00:22:11,000 --> 00:22:16,000 not my forte. Anyhow, here you might see stripes of blue 308 00:22:16,000 --> 00:22:20,000 cells on the skin. The hair won't turn blue actually, 309 00:22:20,000 --> 00:22:25,000 but the skin may if you give it the proper indicator. 310 00:22:25,000 --> 00:22:29,000 And what this indicates is that in this case, the cells that were 311 00:22:29,000 --> 00:22:34,000 injected into the blastocyst could become part of lineages which 312 00:22:34,000 --> 00:22:39,000 committed themselves to becoming skin cells. 313 00:22:39,000 --> 00:22:43,000 Or, the cells in the brain might be blue. Or, the cells in the gut 314 00:22:43,000 --> 00:22:47,000 might be blue. Or under certain conditions, 315 00:22:47,000 --> 00:22:51,000 the cells in the intestine might be blue. In telling you that, 316 00:22:51,000 --> 00:22:55,000 I mean to indicate that the cells that we injected into this 317 00:22:55,000 --> 00:23:00,000 blastocyst, which carry beta-gal were totipotent. 318 00:23:00,000 --> 00:23:04,000 They could create all the tissues of the mouse under the proper 319 00:23:04,000 --> 00:23:08,000 conditions. The proper conditions are obviously being put into this 320 00:23:08,000 --> 00:23:12,000 very special environment in which all kinds of differentiation 321 00:23:12,000 --> 00:23:16,000 inducing signals, which we don't really understand, 322 00:23:16,000 --> 00:23:20,000 can induce this cell to commit itself to enter into one or another 323 00:23:20,000 --> 00:23:24,000 differentiation lineage. And in principal, you can make a 324 00:23:24,000 --> 00:23:28,000 whole organism out of an ES cell. ES cell has as much plasticity, as 325 00:23:28,000 --> 00:23:32,000 much flexibility, as a fertilized egg. 326 00:23:32,000 --> 00:23:36,000 It has not yet lost the ability to make all the parts of the body. 327 00:23:36,000 --> 00:23:40,000 On some occasions, the ES cell will even get into the gonads of the 328 00:23:40,000 --> 00:23:45,000 mouse, which are down here somewhere. And if that's so, 329 00:23:45,000 --> 00:23:49,000 if the ES cell which you injected has been able to seed the formation 330 00:23:49,000 --> 00:23:54,000 of these cells down here, then what will happen is that either 331 00:23:54,000 --> 00:23:58,000 the sperm or the egg coming from this mouse will now transmit 332 00:23:58,000 --> 00:24:04,000 the blue gene. And now, in the next generation, 333 00:24:04,000 --> 00:24:10,000 all of the mice will inherit the blue beta-galactosidase gene in all 334 00:24:10,000 --> 00:24:16,000 of their cells because now this will have entered into the germ line. 335 00:24:16,000 --> 00:24:22,000 If these blue cells happen to colonize the testes, 336 00:24:22,000 --> 00:24:28,000 the ovary, or the testes, then these blue cells will become 337 00:24:28,000 --> 00:24:32,000 ancestors to the sperm or the egg. And now, in the next generation, 338 00:24:32,000 --> 00:24:36,000 mice will inherit a blue gene in all of their cells. 339 00:24:36,000 --> 00:24:40,000 And now this mouse is really happy because it's now part of an 340 00:24:40,000 --> 00:24:44,000 extremely important experiment because now all of its cells will 341 00:24:44,000 --> 00:24:47,000 become blue, having inherited them as part of the oocyte which led to 342 00:24:47,000 --> 00:24:51,000 its formation. In this kind of an animal, 343 00:24:51,000 --> 00:24:55,000 we call this animal a kind of a chimera. Chimera is a mythical 344 00:24:55,000 --> 00:24:59,000 beast which is, let's say, half human and half horse 345 00:24:59,000 --> 00:25:02,000 or something like that. Or a chimera means it has 346 00:25:02,000 --> 00:25:06,000 genetically different parts in it. That is not to say that these parts 347 00:25:06,000 --> 00:25:09,000 carrying the blue gene are necessarily defective, 348 00:25:09,000 --> 00:25:13,000 they're just genetically different, one from the other. But they can 349 00:25:13,000 --> 00:25:16,000 participate in embryogenesis in a fashion that's indistinguishable 350 00:25:16,000 --> 00:25:20,000 from the non-blue cells. They just do everything they're 351 00:25:20,000 --> 00:25:23,000 supposed to do, and they pretend as if they were in 352 00:25:23,000 --> 00:25:27,000 this embryo from the get go, from the very beginning, from the 353 00:25:27,000 --> 00:25:31,000 moment of fertilization. So they are totipotent. 354 00:25:31,000 --> 00:25:34,000 There's an alternative experiment you can do, and you can take the ES 355 00:25:34,000 --> 00:25:38,000 cells, and you can inject them under the skin of a mouse, 356 00:25:38,000 --> 00:25:41,000 let's say. So now, you're putting them in a very unfamiliar 357 00:25:41,000 --> 00:25:45,000 environment. And what you see then on many occasions is you can 358 00:25:45,000 --> 00:25:49,000 actually get a tumor. You can get what's called an 359 00:25:49,000 --> 00:26:00,000 embryonal carcinoma. 360 00:26:00,000 --> 00:26:03,000 Now you'll say, well, so what? That's not so 361 00:26:03,000 --> 00:26:07,000 interesting. But it's very interesting. Why? 362 00:26:07,000 --> 00:26:10,000 Because if you look at the genome of those embryonal carcinoma cells 363 00:26:10,000 --> 00:26:14,000 which we can call EC cells if you want, those cells are genetically 364 00:26:14,000 --> 00:26:17,000 full wild type. And yet, we're getting a tumor here. 365 00:26:17,000 --> 00:26:21,000 So, it means that these cells, which have been placed in a fully 366 00:26:21,000 --> 00:26:24,000 unfamiliar environment under the skin or in the belly of a mouse will 367 00:26:24,000 --> 00:26:28,000 begin to form a tumor. And in fact, they represent the 368 00:26:28,000 --> 00:26:31,000 only type of cell that we know about where a cell having a wild type 369 00:26:31,000 --> 00:26:35,000 genome can actually give you a tumor. 370 00:26:35,000 --> 00:26:39,000 As you sensed from our previous discussions, all other kinds of 371 00:26:39,000 --> 00:26:44,000 human cancer cells we know about have to have mutant genes in order 372 00:26:44,000 --> 00:26:48,000 for them to grow as a malignancy. These cells are fully wild type and 373 00:26:48,000 --> 00:26:53,000 can grow as an embryonal carcinoma. They are very primitive. These 374 00:26:53,000 --> 00:26:57,000 cells have quite a bit of autonomy. They're not so responsive to all 375 00:26:57,000 --> 00:27:02,000 the growth factors that normally are required by many cells throughout 376 00:27:02,000 --> 00:27:07,000 the soma of an animal throughout the tissues. 377 00:27:07,000 --> 00:27:10,000 So this allows us to begin to move on and ask other kinds of questions. 378 00:27:10,000 --> 00:27:14,000 For example, you can take these embryonal carcinoma cells. 379 00:27:14,000 --> 00:27:18,000 You put them in a Petri dish, and you can actually induce them to 380 00:27:18,000 --> 00:27:22,000 differentiate into different cell types in vitro. 381 00:27:22,000 --> 00:27:26,000 How can you do that? Well, we're just beginning to learn 382 00:27:26,000 --> 00:27:30,000 how to do that. We don't really know how to do that. 383 00:27:30,000 --> 00:27:34,000 But, if you give them the right cocktail of growth factors, 384 00:27:34,000 --> 00:27:38,000 they might begin to form muscle cells. If you give them another 385 00:27:38,000 --> 00:27:43,000 cocktail of growth factors, they might begin to give pancreatic 386 00:27:43,000 --> 00:27:47,000 eyelid cells that form insulin, or in this case cartilage cells. 387 00:27:47,000 --> 00:27:52,000 And presumably, the cocktail of growth factors you're providing each 388 00:27:52,000 --> 00:27:56,000 one of these cells with in vitro, i.e. in the Petri dish, is mimicking 389 00:27:56,000 --> 00:28:00,000 the growth factor environment that each of these cell types is 390 00:28:00,000 --> 00:28:04,000 experiencing within the embryo. In other words, 391 00:28:04,000 --> 00:28:08,000 cells in different parts of the embryo experience different 392 00:28:08,000 --> 00:28:12,000 combinations of growth factors that persuade them to commit themselves 393 00:28:12,000 --> 00:28:16,000 to becoming these kind of cells, these kind of cells, and these kind 394 00:28:16,000 --> 00:28:20,000 of cells. And therefore, one of the promises of embryonic 395 00:28:20,000 --> 00:28:24,000 stem cell research is the possibility of being able to 396 00:28:24,000 --> 00:28:28,000 regenerate different kinds of tissues in a fashion that I just 397 00:28:28,000 --> 00:28:32,000 showed you here. But this whole experiment in the 398 00:28:32,000 --> 00:28:36,000 case of human beings is ethically extremely controversial. 399 00:28:36,000 --> 00:28:40,000 Why? Because the experiment starts out making these ES cells here, 400 00:28:40,000 --> 00:28:44,000 and if we want to start out with an early embryo like this, 401 00:28:44,000 --> 00:28:48,000 start out with a blastocyst, in the case of a human blastocyst, 402 00:28:48,000 --> 00:28:52,000 this human blastocyst has the potential under the proper 403 00:28:52,000 --> 00:28:56,000 conditions of becoming a newborn human being. And therefore, 404 00:28:56,000 --> 00:29:00,000 we have this enormous ethical conflict in this country. 405 00:29:00,000 --> 00:29:04,000 Is this blastocyst already a human being? Can you already afford to 406 00:29:04,000 --> 00:29:08,000 truncate the life of this blastocyst at this stage of development, 407 00:29:08,000 --> 00:29:13,000 and in so doing, are you actually extinguishing human life, 408 00:29:13,000 --> 00:29:17,000 or is this organism, if you want to call it that, already still much too 409 00:29:17,000 --> 00:29:22,000 primitive to consider it to be equal to human life? 410 00:29:22,000 --> 00:29:26,000 And here, I would not, unlike my political views, 411 00:29:26,000 --> 00:29:31,000 be forward enough to venture an opinion because it's really 412 00:29:31,000 --> 00:29:35,000 something that no one really can argue about in any objective way. 413 00:29:35,000 --> 00:29:40,000 It's all a matter of opinion. Is this a human being already, 414 00:29:40,000 --> 00:29:44,000 or is it simply an inanimate cluster, a clump of cells? 415 00:29:44,000 --> 00:29:48,000 Now, in principal, how could we do this? 416 00:29:48,000 --> 00:29:52,000 How could we actually create this kind of tissue therapy? 417 00:29:52,000 --> 00:29:56,000 Because the fact is, as you get older, your tissues start falling 418 00:29:56,000 --> 00:30:00,000 apart. You haven't experienced that. 419 00:30:00,000 --> 00:30:04,000 But I have. And the fact is that even if you try to stay in shape, 420 00:30:04,000 --> 00:30:09,000 things just start falling apart. And the older you get, 421 00:30:09,000 --> 00:30:13,000 the more they fall apart. Even people who eat well, 422 00:30:13,000 --> 00:30:18,000 which I do, and exercise well, which I don't, even they fall apart. 423 00:30:18,000 --> 00:30:22,000 And so the question is, are there way of replacing and repairing 424 00:30:22,000 --> 00:30:27,000 tissue? And this would, in principal, represent one such 425 00:30:27,000 --> 00:30:31,000 strategy because it means that you could possibly inject replacement 426 00:30:31,000 --> 00:30:36,000 cells into an agent tissue and generate cells which could then 427 00:30:36,000 --> 00:30:40,000 restore and regeneration function which has somehow inevitably 428 00:30:40,000 --> 00:30:45,000 deteriorated over the decades. Well, that raises the question of 429 00:30:45,000 --> 00:30:50,000 how you can actually get a blastocyst, how you can make a 430 00:30:50,000 --> 00:30:56,000 blastocyst like this. To state an obvious thing which you 431 00:30:56,000 --> 00:31:01,000 might already have intuited, let's say you had such cells 432 00:31:01,000 --> 00:31:05,000 differentiated from various cell types that you want to inject into 433 00:31:05,000 --> 00:31:09,000 somebody's muscle or into their liver if they had diabetes and had 434 00:31:09,000 --> 00:31:13,000 lost their beta cells, or into their cartilage if they 435 00:31:13,000 --> 00:31:17,000 banged up their knee during basketball practice or something 436 00:31:17,000 --> 00:31:21,000 like that, or jogging, which is allegedly good for you. 437 00:31:21,000 --> 00:31:25,000 Who knows? How could you deal with that? Well, the fact is, 438 00:31:25,000 --> 00:31:29,000 let's imagine there were such a blastocyst which we'd produce in 439 00:31:29,000 --> 00:31:34,000 this fashion that we differentiated like this. 440 00:31:34,000 --> 00:31:37,000 OK, this is now the sequence of events. There's an important 441 00:31:37,000 --> 00:31:40,000 consideration we have to take into account, and that is if this 442 00:31:40,000 --> 00:31:44,000 blastocyst came from a different person than you, 443 00:31:44,000 --> 00:31:47,000 and we induced these cells to differentiate, 444 00:31:47,000 --> 00:31:51,000 and we injected those differentiation cells into your 445 00:31:51,000 --> 00:31:54,000 muscle, things wouldn't work. Why? Because these cells, if the 446 00:31:54,000 --> 00:31:57,000 blastocyst originated in a different person than yourself would be 447 00:31:57,000 --> 00:32:01,000 genetically different from you, and would be recognized as foreign 448 00:32:01,000 --> 00:32:04,000 tissue by your immune system. So even though you were getting an 449 00:32:04,000 --> 00:32:08,000 injection of cells which could regenerate your muscle perfectly 450 00:32:08,000 --> 00:32:11,000 well, those cells would never be given a chance to establish 451 00:32:11,000 --> 00:32:15,000 themselves and to thrive, and to reconstruct the tissue simple 452 00:32:15,000 --> 00:32:18,000 because the immune system would regard those cells as being 453 00:32:18,000 --> 00:32:22,000 foreigners and would go after them hammer and tongs trying to get rid 454 00:32:22,000 --> 00:32:25,000 of them in the same way it tries to get rid of all kinds of foreign 455 00:32:25,000 --> 00:32:29,000 invaders. I.e. the only way you could avoid it is 456 00:32:29,000 --> 00:32:33,000 if this blastocyst was genetically identical to you. 457 00:32:33,000 --> 00:32:37,000 But how can you make a blastocyst which is genetically identical to 458 00:32:37,000 --> 00:32:41,000 you? Well, I'm glad I asked that question. That's really the big 459 00:32:41,000 --> 00:32:45,000 challenge we have here because we don't want to create a situation 460 00:32:45,000 --> 00:32:49,000 where we have to restore somebody's tissues, but the only way we can 461 00:32:49,000 --> 00:32:53,000 restore them is to leave them immunosuppressed for the rest of 462 00:32:53,000 --> 00:32:57,000 their lives. When I say immunosuppressed I mean we have to 463 00:32:57,000 --> 00:33:01,000 prevent their immune system from attacking all of these cells that 464 00:33:01,000 --> 00:33:05,000 we've injected in them, these foreign cells, in the same way 465 00:33:05,000 --> 00:33:09,000 that we have to suppress the immune system of any person who has 466 00:33:09,000 --> 00:33:13,000 received a graft from another individual including often bone 467 00:33:13,000 --> 00:33:18,000 marrow transplants. In all cases, we have at least for a 468 00:33:18,000 --> 00:33:24,000 while to prevent their immune system from attacking and eliminating these 469 00:33:24,000 --> 00:33:29,000 engrafted cells. And this is where the whole strategy 470 00:33:29,000 --> 00:33:33,000 comes for the whole process of cloning. You may recall the case of 471 00:33:33,000 --> 00:33:37,000 Dolly about five years ago, and let's remember what happened 472 00:33:37,000 --> 00:33:41,000 here because this would a momentous experiment in mammalian biology. 473 00:33:41,000 --> 00:33:45,000 It asked the question, really, if you take cells from a somatic tissue, 474 00:33:45,000 --> 00:33:49,000 from here, or here, or here, are those cells, 475 00:33:49,000 --> 00:33:53,000 in principal, still totipotent, i.e. is the nucleus, is the genome 476 00:33:53,000 --> 00:33:57,000 of those cells totipotent, or has the genome, the chromosomal 477 00:33:57,000 --> 00:34:01,000 complement of cells in their cells undergone some kind of irrevocable, 478 00:34:01,000 --> 00:34:05,000 irreversible change, which precludes those cells from ever 479 00:34:05,000 --> 00:34:08,000 becoming totipotent? Well, in fact, 480 00:34:08,000 --> 00:34:12,000 if you take mammary epithelial cells from the breast of a human being or 481 00:34:12,000 --> 00:34:15,000 from the breast of a ewe and you put them into the blastocyst, 482 00:34:15,000 --> 00:34:18,000 nothing's going to happen. Those introduced mammary epithelial 483 00:34:18,000 --> 00:34:22,000 cells will not be able to establish themselves in the blastocyst. 484 00:34:22,000 --> 00:34:25,000 And, we will not be able to insinuate themselves amidst the 485 00:34:25,000 --> 00:34:29,000 inner cell mass, and they will not be able to 486 00:34:29,000 --> 00:34:33,000 participate in embryogenesis. So therefore, the epigenetic program 487 00:34:33,000 --> 00:34:38,000 in these somatic cells seems to be irrevocably set to preclude the 488 00:34:38,000 --> 00:34:44,000 participation of the already differentiated mammary epithelial 489 00:34:44,000 --> 00:34:49,000 cells in subsequent embryogenesis. Therefore, you could not do this 490 00:34:49,000 --> 00:34:54,000 experiment all over again of introducing cells into the inner 491 00:34:54,000 --> 00:35:00,000 cell mass as I just described over here, injecting them into this. 492 00:35:00,000 --> 00:35:04,000 But still, that doesn't answer the question. The issue is not whether 493 00:35:04,000 --> 00:35:08,000 the mammary epithelial cell is irrevocably committed to being a 494 00:35:08,000 --> 00:35:12,000 mammary epithelial cell. The issue: is its genome capable 495 00:35:12,000 --> 00:35:16,000 under the proper circumstances of becoming an early embryonic cell. 496 00:35:16,000 --> 00:35:21,000 And therefore, what was done is the following. One took mammary 497 00:35:21,000 --> 00:35:25,000 epithelial cells, in this case from Dolly's quote 498 00:35:25,000 --> 00:35:29,000 unquote "mother, one prepared nuclei from these 499 00:35:29,000 --> 00:35:33,000 cells, taking them out of the cytoplasm, and then one got 500 00:35:33,000 --> 00:35:38,000 fertilized eggs or eggs that have been induced to become. 501 00:35:38,000 --> 00:35:42,000 So here's an oocyte. An oocyte is an unfertilized egg. 502 00:35:42,000 --> 00:35:46,000 In principle, you can activate an oocyte by putting a sperm in, 503 00:35:46,000 --> 00:35:51,000 or in fact it's actually better if you take the oocyte and you fool it 504 00:35:51,000 --> 00:35:55,000 into thinking it's become fertilized by treating it with different salts, 505 00:35:55,000 --> 00:36:00,000 high potassium concentration, and so forth. 506 00:36:00,000 --> 00:36:04,000 And that will induce the egg to say I've been fertilized. 507 00:36:04,000 --> 00:36:09,000 I better start embryogenesis. But what you do in this case is the 508 00:36:09,000 --> 00:36:13,000 following. The egg has its own haploid nucleus here, 509 00:36:13,000 --> 00:36:18,000 and you can take a little needle. And, you suck that nucleus right 510 00:36:18,000 --> 00:36:23,000 out of the egg. So, you've enucleated it. 511 00:36:23,000 --> 00:36:27,000 That's what you've done, and now the egg is enucleate. 512 00:36:27,000 --> 00:36:32,000 It doesn't have a nucleus in it. But keep in mind, 513 00:36:32,000 --> 00:36:36,000 much of what happens during early embryogenesis is programmed not only 514 00:36:36,000 --> 00:36:41,000 by the genes but by all array of cytoplasmic proteins that are 515 00:36:41,000 --> 00:36:46,000 present throughout the egg, and which play critical roles in 516 00:36:46,000 --> 00:36:50,000 determining the subsequent course of embryogenesis. 517 00:36:50,000 --> 00:36:55,000 So now what you can do is you inject into this enucleate oocyte 518 00:36:55,000 --> 00:37:00,000 the nucleus of a mammary epithelial cell. 519 00:37:00,000 --> 00:37:05,000 The mammary epithelial cell is obviously highly differentiated. 520 00:37:05,000 --> 00:37:10,000 It's there to make milk. We'll call it an MEC if you want, 521 00:37:10,000 --> 00:37:15,000 and you put that in there, and under certain circumstances, 522 00:37:15,000 --> 00:37:20,000 and then you can treat this with a little bit of salt to mimic the 523 00:37:20,000 --> 00:37:25,000 physiological stimulus that comes after the sperm hits the egg. 524 00:37:25,000 --> 00:37:31,000 And now this egg will think it's been fertilized. 525 00:37:31,000 --> 00:37:35,000 And now it will begin to divide. But keep in mind, the genome of 526 00:37:35,000 --> 00:37:39,000 this quote unquote "unfertilized egg" has come not from the sperm and 527 00:37:39,000 --> 00:37:44,000 the preexisting nucleus of the egg. It's come because the nucleus has 528 00:37:44,000 --> 00:37:48,000 been injected from a mammary epithelial cell. 529 00:37:48,000 --> 00:37:52,000 An experience over the last 30 years had indicated that this will 530 00:37:52,000 --> 00:37:57,000 never work. But finally somebody in Scotland, a man named Ian Wilmouth 531 00:37:57,000 --> 00:38:01,000 tinkered enough with the conditions of these cells that he could 532 00:38:01,000 --> 00:38:05,000 actually get it to work not so often, maybe one, or two, 533 00:38:05,000 --> 00:38:10,000 or three times out of 100 tries. But on those conditions, 534 00:38:10,000 --> 00:38:14,000 this thing would begin to divide. The nucleus would begin to divide 535 00:38:14,000 --> 00:38:19,000 its diploid. Keep in mind that when a sperm comes into an egg, 536 00:38:19,000 --> 00:38:23,000 the egg is haploid. The sperm is haploid. Together they make a 537 00:38:23,000 --> 00:38:27,000 diploid genome. This introduced genomus diploid, 538 00:38:27,000 --> 00:38:32,000 and the question is, the critical question is, can the genes in this 539 00:38:32,000 --> 00:38:36,000 introduced nucleus totally rearrange their transcriptional program so 540 00:38:36,000 --> 00:38:41,000 that even though these genes might all be intact in terms of nucleotide 541 00:38:41,000 --> 00:38:45,000 sequence, can the entire infinitely complex array of DNA associated 542 00:38:45,000 --> 00:38:50,000 proteins, I.e. the proteins that constitute 543 00:38:50,000 --> 00:38:54,000 the chromatin which is not only the histones but also the transcription 544 00:38:54,000 --> 00:38:59,000 factors, the TF's, can they all jump on and jump off as 545 00:38:59,000 --> 00:39:03,000 they should to mimic and replicate the spectrum of transcription 546 00:39:03,000 --> 00:39:08,000 factors that is normally present shortly after an egg is fertilized? 547 00:39:08,000 --> 00:39:12,000 If they can do that, then this embryo can begin to 548 00:39:12,000 --> 00:39:16,000 replicate, and can ultimately develop into a complete embryo. 549 00:39:16,000 --> 00:39:20,000 If they can't, then embryogenesis is going to be truncated shortly 550 00:39:20,000 --> 00:39:24,000 thereafter maybe at the two cell stage, at the four cell stage, 551 00:39:24,000 --> 00:39:28,000 at the 16 cell stage, but shortly thereafter, not because of the DNA 552 00:39:28,000 --> 00:39:32,000 sequences being defective, but because the spectrum of 553 00:39:32,000 --> 00:39:36,000 transcription factors is up and down regulates certain genes is in fact 554 00:39:36,000 --> 00:39:40,000 not been able to re-assort themselves in response to what? 555 00:39:40,000 --> 00:39:44,000 Initially, in response to the signals coming from the cytoplasm 556 00:39:44,000 --> 00:39:48,000 because one might imagine, correctly so, that the nucleus in 557 00:39:48,000 --> 00:39:53,000 here is getting signals from the cytoplasm telling it, 558 00:39:53,000 --> 00:39:57,000 in effect, telling this nucleus, you should behave functionally as if 559 00:39:57,000 --> 00:40:01,000 you were the nucleus of a fertilized egg. In other words, 560 00:40:01,000 --> 00:40:05,000 the environment of proteins here is influencing the behavior 561 00:40:05,000 --> 00:40:09,000 of this nucleus. That goes backwards to our normal 562 00:40:09,000 --> 00:40:12,000 way of thinking because keep in mind our normal vectoral way of thinking 563 00:40:12,000 --> 00:40:14,000 is that the nucleus is influencing the cytoplasm. 564 00:40:14,000 --> 00:40:17,000 That's the direction of information flow. But here, 565 00:40:17,000 --> 00:40:20,000 we're having a different situation. Here, the cytoplasm is telling this 566 00:40:20,000 --> 00:40:23,000 injected nucleus, well, you used to be a mammary 567 00:40:23,000 --> 00:40:25,000 epithelial cell nucleus, but now you've got to take on a 568 00:40:25,000 --> 00:40:28,000 different job. And we're going to force you to do 569 00:40:28,000 --> 00:40:32,000 so. And to the extent that happens, 570 00:40:32,000 --> 00:40:36,000 then in principle, one can end up having a normal embryo. 571 00:40:36,000 --> 00:40:40,000 And, it happened actually on rare occasion that this worked. 572 00:40:40,000 --> 00:40:44,000 Here they used actual electrical stimulus rather than salt to get the 573 00:40:44,000 --> 00:40:48,000 nucleus to divide. This electrical stimulus, 574 00:40:48,000 --> 00:40:52,000 again, was to mimic the stimulus that the sperm entering the egg 575 00:40:52,000 --> 00:40:56,000 normally provides, thereby activating the egg and 576 00:40:56,000 --> 00:41:00,000 forcing the entire fertilized egg to proliferate. 577 00:41:00,000 --> 00:41:03,000 And so, once this starts developing, let's say, the blastocyst stage, 578 00:41:03,000 --> 00:41:07,000 here we have a blastocyst. You can see the inner cell mass 579 00:41:07,000 --> 00:41:11,000 once again here. This can be transferred into a 580 00:41:11,000 --> 00:41:14,000 pseudo-pregnant ewe. Pseudo-pregnant means you take a 581 00:41:14,000 --> 00:41:18,000 female ewe and you inject it with a series of hormones that persuade her 582 00:41:18,000 --> 00:41:22,000 reproductive system including prolactin, and progesterone, 583 00:41:22,000 --> 00:41:25,000 or estrogen, persuade her reproductive system, 584 00:41:25,000 --> 00:41:29,000 her uterus, that she's pregnant. You inject this early embryo into 585 00:41:29,000 --> 00:41:33,000 her, and this early embryo will then implant into the wall of her uterus 586 00:41:33,000 --> 00:41:37,000 and begin to develop. And if it all works well, 587 00:41:37,000 --> 00:41:41,000 you get a Dolly is born. You get a new sheep coming out of this. 588 00:41:41,000 --> 00:41:46,000 It doesn't work so often, one, two, three, four times after out of 589 00:41:46,000 --> 00:41:50,000 a hundred, and very often in the great majority of cases, 590 00:41:50,000 --> 00:41:55,000 there are mis-births, mis-carriages, which happen in the middle of 591 00:41:55,000 --> 00:41:59,000 embryogenesis. So, almost in the great majority of 592 00:41:59,000 --> 00:42:04,000 cases, this fails. Somehow, the reprogramming of this 593 00:42:04,000 --> 00:42:08,000 nucleus, which is what we're talking about, reprogramming it in terms of 594 00:42:08,000 --> 00:42:12,000 its transcriptional program, goes awry. And therefore, bad 595 00:42:12,000 --> 00:42:17,000 things happen. The fact that on a rare occasion 596 00:42:17,000 --> 00:42:21,000 gets and succeeds here already is extremely interesting because it 597 00:42:21,000 --> 00:42:25,000 proves irrevocably that the genome of a mammary epithelial cell is in 598 00:42:25,000 --> 00:42:30,000 principle competent to program entire embryonic development. 599 00:42:30,000 --> 00:42:34,000 And that means that during the development of Dolly's mother, 600 00:42:34,000 --> 00:42:39,000 we'll put her up here, as she developed from one cell into 1, 601 00:42:39,000 --> 00:42:44,000 00 or 10,000 billion cells, as that development occurred the DNA 602 00:42:44,000 --> 00:42:49,000 sequences that went from the fertilized egg to her didn't really 603 00:42:49,000 --> 00:42:53,000 change. I.e. the DNA sequences that were in one of her mammary 604 00:42:53,000 --> 00:42:58,000 epithelial cells were intact, and as capable in principle of 605 00:42:58,000 --> 00:43:03,000 launching the full-fledged development as would be 606 00:43:03,000 --> 00:43:08,000 a fertilized egg. And that is one of the proofs, 607 00:43:08,000 --> 00:43:12,000 by the way, that in fact differentiation does not involve, 608 00:43:12,000 --> 00:43:16,000 with some rare exceptions, alterations in DNA sequence. 609 00:43:16,000 --> 00:43:20,000 This, in turn, ends up being connected with the whole issue of 610 00:43:20,000 --> 00:43:24,000 embryonic stem cells. Let's say that I wanted to have my 611 00:43:24,000 --> 00:43:28,000 muscles regenerated, although they're still pretty good. 612 00:43:28,000 --> 00:43:33,000 So, I take a skin cell of mine, and I inject the skin cell. 613 00:43:33,000 --> 00:43:36,000 I take the nucleus out, and I inject it into an oocyte. 614 00:43:36,000 --> 00:43:40,000 And then I let the oocyte develop up to this stage. 615 00:43:40,000 --> 00:43:44,000 And I don't put the oocyte back into a sheep or another woman, 616 00:43:44,000 --> 00:43:48,000 although I could in principle. I actually take the cells out of the 617 00:43:48,000 --> 00:43:51,000 inner cell mass. Those are ES cells, 618 00:43:51,000 --> 00:43:55,000 and I begin to use them to regenerate my muscles to do this 619 00:43:55,000 --> 00:43:59,000 strategy. So, the cells are, in this case, 620 00:43:59,000 --> 00:44:03,000 not used for reproductive cloning, which is what this is here. 621 00:44:03,000 --> 00:44:07,000 They're used for therapeutic cloning, where instead of taking these cells 622 00:44:07,000 --> 00:44:11,000 and the ES cells and allowing them to form a whole embryo, 623 00:44:11,000 --> 00:44:15,000 they're used to form a cell line of ES cells from the blastocyst from 624 00:44:15,000 --> 00:44:19,000 the inner cell mass. What we talked about before, 625 00:44:19,000 --> 00:44:23,000 here you see the blastocyst with the inner cell mass here. 626 00:44:23,000 --> 00:44:27,000 You see it again. But now, rather than allowing this blastocyst 627 00:44:27,000 --> 00:44:31,000 to continue development, we simply extract cells from it and 628 00:44:31,000 --> 00:44:34,000 again create ES cells. I could create therefore in 629 00:44:34,000 --> 00:44:38,000 principle, ES cells, which are genetically identical to 630 00:44:38,000 --> 00:44:41,000 all the cells in my body, and any one of you could as well. 631 00:44:41,000 --> 00:44:44,000 And here, there's not only one, but there's two ethical complications. 632 00:44:44,000 --> 00:44:48,000 First of all, here we're starting human life with the intent of 633 00:44:48,000 --> 00:44:51,000 truncating it very early, and secondly, where are the oocytes 634 00:44:51,000 --> 00:44:54,000 going to come from? Well, you could say you can get 635 00:44:54,000 --> 00:44:58,000 them from some women, but producing oocytes from a human 636 00:44:58,000 --> 00:45:02,000 female isn't so easy. You have to inject her with all 637 00:45:02,000 --> 00:45:06,000 kinds of stimulatory hormones, choreogramatatrophic hormones. It's 638 00:45:06,000 --> 00:45:10,000 an unpleasant procedure. Usually women are paid $5, 639 00:45:10,000 --> 00:45:14,000 00 or $10,000 to produce some oocytes. Well, 640 00:45:14,000 --> 00:45:18,000 you say, that's OK, but is that OK? I don't know. 641 00:45:18,000 --> 00:45:22,000 Is it OK to pay a woman to donate her oocytes to make herself into an 642 00:45:22,000 --> 00:45:26,000 oocyte factory? I don't know. You have to judge. 643 00:45:26,000 --> 00:45:30,000 I think there's arguments both for and against it. 644 00:45:30,000 --> 00:45:34,000 Clearly, any one of us would be extraordinarily naïve if we thought 645 00:45:34,000 --> 00:45:39,000 that this was a procedure which had no ethical encumbrances in it. 646 00:45:39,000 --> 00:45:43,000 And, you have to think about them for yourself. Still, 647 00:45:43,000 --> 00:45:48,000 the potentials are enormous, and therefore the question exists. 648 00:45:48,000 --> 00:45:53,000 Will there be ways in the future of taking differentiated cells from 649 00:45:53,000 --> 00:45:57,000 one's tissue, and in fact using them in these ways to make ES cells 650 00:45:57,000 --> 00:46:02,000 without having to go through an oocyte, and without having the 651 00:46:02,000 --> 00:46:06,000 potential of creating human life. The alternative to this has been to 652 00:46:06,000 --> 00:46:10,000 do the following, to go into our normal tissues and 653 00:46:10,000 --> 00:46:14,000 pull out adult stem cells. What do I mean by adult stem cells? 654 00:46:14,000 --> 00:46:18,000 These are not stem cells that are totipotent. These are stem cells 655 00:46:18,000 --> 00:46:22,000 which are in my muscles and regenerating muscle mass, 656 00:46:22,000 --> 00:46:26,000 which happens believe it or not. These are stem cells which might be 657 00:46:26,000 --> 00:46:30,000 in my skin and are continually regenerating skin cells. 658 00:46:30,000 --> 00:46:34,000 Keep in mind that in the maintenance of all our normal tissues there are 659 00:46:34,000 --> 00:46:38,000 stem cells whose configuration can formally be depicted like this with 660 00:46:38,000 --> 00:46:42,000 the transit amplifying cells we talked about before. 661 00:46:42,000 --> 00:46:46,000 And maybe, if one took the stem cells out of an adult tissue right 662 00:46:46,000 --> 00:46:50,000 here, if we had a way of extracting them, those could be propagated in 663 00:46:50,000 --> 00:46:54,000 vitro, and then injected back in. Those are so-called adult stem 664 00:46:54,000 --> 00:46:58,000 cells. And the individuals who are against 665 00:46:58,000 --> 00:47:02,000 this kind of manipulation of human embryos and so forth say that adult 666 00:47:02,000 --> 00:47:06,000 stem cells are really the solution. You take stem cells out of a 667 00:47:06,000 --> 00:47:10,000 person's tissue, you expand them. Ex vivo means out 668 00:47:10,000 --> 00:47:14,000 of the body, in vitro, and then you use them. You inject 669 00:47:14,000 --> 00:47:19,000 them into somebody's tissue to regenerate their tissue. 670 00:47:19,000 --> 00:47:23,000 There's only one problem with that. It's ethically far less encumbered 671 00:47:23,000 --> 00:47:27,000 obviously, but it doesn't work that well. In fact, 672 00:47:27,000 --> 00:47:31,000 some people think it hardly works at all, that the exceptions are really 673 00:47:31,000 --> 00:47:36,000 rather far and few between. And so, this issue will long be or 674 00:47:36,000 --> 00:47:41,000 continue to be debated. But it obviously represents a very 675 00:47:41,000 --> 00:47:46,000 new and exciting area of biomedical research. And interestingly enough, 676 00:47:46,000 --> 00:47:52,000 it impinges as well in a fully unexpected way on cancer because 677 00:47:52,000 --> 00:47:57,000 this whole paradigm of stem cells, it turns out, also applies to cancer 678 00:47:57,000 --> 00:48:01,000 cells. If you were to have asked me two or 679 00:48:01,000 --> 00:48:05,000 three years ago, what did the cells in the tumor look 680 00:48:05,000 --> 00:48:09,000 like? I would draw a picture like this, that these are a series of 681 00:48:09,000 --> 00:48:12,000 exponentially growing cells so that all the cancer cells, 682 00:48:12,000 --> 00:48:16,000 all the neoplastic cells in the tumor mass are biologically 683 00:48:16,000 --> 00:48:20,000 equivalent to one another. They all have the same mutant 684 00:48:20,000 --> 00:48:23,000 genome, and they all are capable of multiplying exponentially. 685 00:48:23,000 --> 00:48:27,000 But it turns out that work in the Matavoidic system on Matevoidic 686 00:48:27,000 --> 00:48:31,000 tumors like leukemias, and now on breast cancers, 687 00:48:31,000 --> 00:48:36,000 yields a very different results, because it turns out that the way 688 00:48:36,000 --> 00:48:44,000 that the tumors are organized looks like this. The tumors also are 689 00:48:44,000 --> 00:48:52,000 organized in this hierarchical array just like normal tissue. 690 00:48:52,000 --> 00:49:00,000 How do we know that? Again, I'm glad I asked that question. 691 00:49:00,000 --> 00:49:04,000 Because if you take these cells out of the tumor and put them in another 692 00:49:04,000 --> 00:49:08,000 mouse, let's say, you get a new tumor. 693 00:49:08,000 --> 00:49:13,000 These cells are tumorogenic, I.e. they concede a new tumor. 694 00:49:13,000 --> 00:49:17,000 If you take these cells out of the tumor, they have the same mutant 695 00:49:17,000 --> 00:49:21,000 genome. They constitute the bulk, the vast mass of the cancer cells in 696 00:49:21,000 --> 00:49:26,000 a tumor. You put these into a mouse, and they're non-tumorogenic. 697 00:49:26,000 --> 00:49:30,000 And, in some kinds of tumors, the tumorogenic cells can represent 698 00:49:30,000 --> 00:49:35,000 only 1 or 2% of the total mass of cancer cells in the tumor. 699 00:49:35,000 --> 00:49:38,000 And from this, we begin to realize that you look 700 00:49:38,000 --> 00:49:42,000 inside tumors: the tumors deviate minimally from the organization of 701 00:49:42,000 --> 00:49:46,000 normal tissue. They also depend on self-renewing 702 00:49:46,000 --> 00:49:50,000 stem cells which can make transit amplifying cells and can give end 703 00:49:50,000 --> 00:49:53,000 stage cells, which although they're neoplastic, have many of the 704 00:49:53,000 --> 00:49:57,000 differentiated characteristics of the normal tissue from which they 705 00:49:57,000 --> 00:50:01,000 arose. And this has enormous implications for, 706 00:50:01,000 --> 00:50:05,000 for example, therapies against tumors. 707 00:50:05,000 --> 00:50:09,000 If you ask somebody, how do you develop and how you judge 708 00:50:09,000 --> 00:50:13,000 the success of an anticancer treatment? You talk to somebody 709 00:50:13,000 --> 00:50:17,000 like from the pharmaceutical industry. And let's say that's easy. 710 00:50:17,000 --> 00:50:21,000 If you have a new drug, and that drug reduces the mass of a 711 00:50:21,000 --> 00:50:26,000 tumor by 50%, that means that you've done something really good. 712 00:50:26,000 --> 00:50:30,000 But let's look what's going on here. If these cells are 99% of the tumor 713 00:50:30,000 --> 00:50:34,000 in terms of the mass and these cells are 1% of the tumor, 714 00:50:34,000 --> 00:50:38,000 let's say you've invented a new drug which wipes out all of these cells 715 00:50:38,000 --> 00:50:42,000 but doesn't touch these cells. The bulk of the tumor has shrunk and 716 00:50:42,000 --> 00:50:46,000 everybody will say, eureka, we've succeeded in curing 717 00:50:46,000 --> 00:50:50,000 cancer. But keep in mind that the self-renewing capacity of the tumor 718 00:50:50,000 --> 00:50:53,000 rests in these cells. And if these cells are allowed to 719 00:50:53,000 --> 00:50:57,000 survive, then they'll start proliferating again and regenerate 720 00:50:57,000 --> 00:51:01,000 the entire tumor mass. And you won't really know that you 721 00:51:01,000 --> 00:51:05,000 had any success because these cells look like all the other tumor cells 722 00:51:05,000 --> 00:51:10,000 under the microscope. But biologically, they're very 723 00:51:10,000 --> 00:51:14,000 different. And therefore, the future of cancer therapy, 724 00:51:14,000 --> 00:51:19,000 and it will take five or ten years to do this, has to begin to focus on 725 00:51:19,000 --> 00:51:23,000 getting rid of these self-renewing stem cells which create this 726 00:51:23,000 --> 00:51:28,000 enormous regenerative capacity on the part of tumors. 727 00:51:28,000 --> 00:51:32,000 See you next Monday. Have a great vacation. 728 00:51:32,000 --> 00:51:37,000 Eat much turkey, and get some exercise, and don't smoke.