A Critique of Pure (Genetic) Information

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116 Chapter 3 primacy then any explanatory account must place all its cards on the table. When the conflationary temptation to pack contingent developmental outcomes into the one-dimensional sequence arrays of polymers is set aside, then the coding sequences of DNA may be reconceptualized as one type of resource among many, i.e., as Gene-D (Moss 2001). Beyond just a formal parity of resources, DST provides a new opening within which the relationship between different hierarchical orders of the living world may be reconceptualized.
4 Dialectics of Disorder: Normalization and Pathology as Process Epigenetics (Waddington’s term for the analytical study of individual development) can shed light on the process of tumorigensis, and vice versa. —Julian Huxley, 1958 Overgrowth or dedifferentiation are effects of . . . disorganization—repercussions not driving forces. Cancer is no more a disease of cells than a traffic jam is a disease of cars. A lifetime of study of the internal-combustion engine would not help anyone to understand our traffic problems. The causes of congestion can be many. A traffic jam is due to a failure of the normal relationship between driven cars and their environment and can occur whether they themselves are running normally or not . . . Cancer is a disease of organization, not a disease of cells... What we need most at present is to develop an autonomous science of organismal organization, the social science of the human body; a science not so naïve as to suppose that its units, when isolated, will behave exactly as they do in the context of the whole of which they form a part, and willing to recognize that whole functioning organisms are its proper concern. I will try to explain normal growth, differentiation, maintenance, and repair, as well as their disorder. It will take biological orderliness in action as its field of study. It lies, in wait for a name, between cytology and sociology. It is much more than oncology, for it is the study of the organization of whole organisms as well as that of disorganisational tumour formation. —D. W. Smithers, 1962 It is well known from classic genetics that the expression of any multigenic phenomenon is very dependent on the genotypic milieu, so that a given mutation may be deleterious in one genetic milieu and advantageous in another. Thus, the combination of mutagenic changes in genotypic milieus which are different in every human, plus the sensitivity of multigenic phenotypes to the surrounding environment, account for the difficulty in predicting the likelihood of nonfamilial or sporadic cancers or their outcome once they appear....Even where there is a dominant germ line mutation that favors development of cancer with
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What Genes Can’t Do
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What Genes Can’t Do Lenny Moss A
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To my daughters, Julie and Rachel
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Series Foreword We are pleased to p
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Introduction There can be little do
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Introduction xv argument was mistak
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Introduction xvii The empirical fru
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Introduction xix Schrödinger, rely
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What Genes Can’t Do
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2 Chapter 1 ubiquitous types of mol
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4 Chapter 1 The Phylogenetic Turn a
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6 Chapter 1 achievement of an ontog
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8 Chapter 1 do it. The most vituper
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10 Chapter 1 3. The parts of the tr
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12 Chapter 1 Judgment). Kant famous
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14 Chapter 1 Figure 1.1 Von Baer’
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16 Chapter 1 “embryological metho
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18 Chapter 1 activity was under the
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20 Chapter 1 established. Recalling
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22 Chapter 1 Charles Otis Whitman w
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24 Chapter 1 hybrids, Mendel’s in
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26 Chapter 1 variation was largely
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28 Chapter 1 simplify further the e
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30 Chapter 1 compromising ante-act,
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32 Chapter 1 hypothesis, cellular d
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34 Chapter 1 “merogony” experim
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36 Chapter 1 no means presupposed a
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38 Chapter 1 he turned to Johannsen
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40 Chapter 1 remainder of DNA is go
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42 Chapter 1 Johannsen reproduces i
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44 Chapter 1 context-specific inter
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46 Chapter 1 normal sequence resour
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48 Chapter 1 priority of causal det
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50 Chapter 1 simultaneously investe
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52 Chapter 2 spectrum of different
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54 Chapter 2 (Gene-D) in a renewed
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56 Chapter 2 i.e., the acquisition,
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58 Chapter 2 Atomic configurations,
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60 Chapter 2 “aperiodic solids,
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62 Chapter 2 of the self-executing
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64 Chapter 2 Gamow’s Translation
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Page 94 and 95: 76 Chapter 3 Taking Schrödinger Se
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Page 102 and 103: 84 Chapter 3 protein that ultimatel
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Page 110 and 111: 92 Chapter 3 The cell’s system of
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Page 118 and 119: 100 Chapter 3 that homeostatic, aut
Page 120 and 121: 102 Chapter 3 The pertinent questio
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Page 156 and 157: 138 Chapter 4 A DNA probe must sati
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166 Chapter 4 capsule of an adult m
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168 Chapter 4 in three ways: (1) Re
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170 Chapter 4 The earlier nodules,
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172 Chapter 4 When Rubin’s cells
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174 Chapter 4 sporadically. Epidemi
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176 Chapter 4 such as that of the D
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178 Chapter 4 What constitutes then
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180 Chapter 4 about by way of the c
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182 Chapter 4 because the epidemiol
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184 Chapter 5 genome structure. ...
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186 Chapter 5 Neither humans nor hi
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188 Chapter 5 is thought to be at l
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190 Chapter 5 that the absence (or
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192 Chapter 5 steps. In the first s
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194 Chapter 5 certain Gene-D into a
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196 Chapter 5 place, as it were, be
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198 Chapter 5 The decay and demise
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200 Notes to pages 12-42 preformed
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202 Notes to pages 113-184 4. Human
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206 References Blau, H., Chiu, C.,
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208 References Gamow, G. (1954),
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210 References Keller, E. F. (2001)
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212 References Poo, C. (1974), “L
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214 References Stern, C. and Sherwo
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218 Index Birthmarks (nevi), 128 Bi
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220 Index Conklin, Edwin, 34-35, 36
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222 Index Gene-P. See Gene-P/Gene-D
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224 Index Idioplasm, 31-33, 34 Impr
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226 Index Parasitism (symbiotic mod
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228 Index Vogt, O., 200n.13 von Bae
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