Text 1113, 171 rader
Skriven 2004-12-20 06:18:00 av Cncabej (1:278/230)
Ärende: "Genes are followers not
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(The title of this post is based on West-Eberhard's view on the relative role
of genes in heredity and evolution as expressed in her Developmental Plasticity
and Evolution (2003), an excellent book that, in Prof. Nijhout's opinion "may
prove to be the most important and insightful book about evolution since "The
Origin of Species").

I thank P. Fellini for inviting me to present here in sbe my views on what he
chose to call "alluring (necessarily/realistically tenuous) proposition". 
Peter, I thought a little about it and concluded that I could make my view
clear in the process: by  first challenging the status of the prevailing gene
theory as a theory of heredity in metazoans and then presenting ESSENTIALS
(constrained by space limitations and other issues in sbe) of my alternative
view. In the course of discussions readers could create their opinion on the
relative merits of each theory and the degree to which each of them reflects
the real state of things in the living world. 

The role of genes in heredity is becoming probably the most controversial issue
in modern biology. The majority of leading biologists still believe that genes
determine the heredity of all the living organisms and their evolution is
essentially the evolution of their genes (now the words genetics and genetical
have become synonymous to heredity and hereditary!). On the other pole there is
a growing minority of distinguished biologists that do not endorse that view,
or even reject it, insisting that genes do not do more than what is
experimentally known they do: provide information for protein biosynthesis.

Personally, I don't believe we have seen the facts or heard reasons why genes
must be considered to be determinants of heredity and the "raw material of
evolution". We are told that evolution of a gene (not just any change), takes
evolutionarily considerable periods of time, that evolution of a structure may
need evolution of a varying number of genes, and evolution of a new organ
requires evolution of an even greater number of genes and longer periods of
time. Accordingly, it is to be expected that evolution of a new Bauplan for
transition from a class, such as fishto amphibians, requires evolution of a
still larger number of genes and longer periods of time. Have we proven this?
Certainly not. It is true that amphibians and fishes differ in their genes, but
the occurrence of evolution of amphibian (and fish) genes is not proof that
they have determined the evolution of Amphibia. Remember West-Eberhard: genes
may be followers, not leaders of evolution: all the observed evolution of their
genes may have taken place after the evolution of the class of amphibians.
 
Indeed, why on the earth would evolution of those animals require changes in
their genes when with the same set of genes they are able, within their life
cycle, to not only modify a structure or form a new organ but create two
different Bauplaene (fish and amphibian or worm and insect)?

Here in sbe differences of views also exist on the relative role of genes.

In my opinion, an objective examination of the epistemological status of the
gene theory clearly shows that it has failed in explaining:
- How could genetic information that determines amino acid sequence also
determine the complex and highly specific spatial arrangement of cells of
various types from which metazoan morphology arises? 
- Where the enormous amount of information (of the order of trillions of bits)
necessary for erecting a metazoan structure comes from? 
- Where the information for turning on/off nonhousekeeping genes that determine
cell differentiation during the development comes from.

The best we have heard so far are tautological speculations of the type of
self-assembly etc., which require explanations themselves.

What I propose here, instead, is an alternative theory of heredity in
metazoans, whose main theses could be summarized as follows:

1. Any material system, however simple it might be, sooner or later will lose
their identity if not externally regulated. Man-made systems also need human
intervention or appropriate control systems in order to maintain their
structure. Being incomparably more complex than any other material system and
than any system human genius has been able to create, metazoans also need and
have control systems for maintaining their structure and function.
2. A system of heredity, by definition is a control system that maintains the
structure and function of living systems. 
3. The control system in unicellulars is represented by the genome (acting as
controller of the control system), the apparatus for transcription and
translation of genetic information, and the metabolic machinery of the cell.
4. During the reproduction in unicellulars, their control system functions as a
genetic (Watson-Crick) system of heredity.
5. An integrated control system (ICS), with the central nervous system (CNS) as
its controller, maintains the structure and functions in metazoans
6. During reproduction, in metazoans that system also functions as their
epigenetic system of heredity; it controls and regulates all the stages of
individual development (gametogenesis, early embryonic development, and
postphylotypic development). 

The hypothesis, in which form this theory was first presented, allowed to make
the following predictions:
1. Expression of nonhousekeeping genes in metazoans is controlled and regulated
by signal cascades originating in the CNS
2. Initial signals, or the information, for starting signal cascades in the CNS
are not of genetic, but of computational, i.e. epigenetic, origin.
3. The reproduction cycle and gametogenesis, production of egg- and sperm
cells, in metazoans are under control of the epigenetic system of heredity,
with the CNS as generator of epigenetic information.
4. The transfer of the epigenetic information (maternal cytoplasmic factors and
geneimprinting) in gametes is under control of the parental epigenetic
system(s) of heredity.
5. At the phylotypic stage, when the function of maternal cytoplasmic factors
terminates, the embryonic CNS is operational and takes over the control of
embryonic development.
6. All signal cascades determining the postphylotypic development up to
adulthood originate in the CNS.

Ever since, I have found that all those predictions can be substantiated by
adequate empirical evidence. Now, the epigenetic theory of heredity offers a
novel and empirically validated explanans for the inheritance in metazoans. The
theory makes possible rational explanations of most of the phenomena that the
gene theory has clearly failed to do so far (the sudden morphological changes
without changes in genes, the widespread phenomena of alternative  phenotypes,
sudden speciation, sudden reversion to the ancestral traits of million years
ago, evolutionary convergence, etc.) 

Even though adequately verified, the epigenetic theory of heredity is open to
scientific inquiry and can be further experimentally verified/falsified.

Constrained by limitations of postings in sbe, I have only presented herein the
theoretical pillars of the epigenetic theory of heredity, which offer but the
most general idea on the nature of the theory and pointed out the fundamental
distinction of this theory from the prevailing genetic theory of heredity. I
hope that here in sbe the main features of the epigenetic system of heredity
may be unfolded in the course of discussions on the theory and the following
(undoubtedly) controversial comparison of the explanatory power of both
theories.
 
A basic comparison between the genetic and epigenetic theories of heredity
seems to demonstrate that the latter has essentially succeeded, while the first
fails, to provide experimentally verifiable answers to the following basic
requirements for any system of heredity: 

1. To present a discrete mechanism, showing the origin of signal cascades
leading to formation of an organ or another structure, in the process of
individual development is necessary for validating any theory that claims to be
a theory of heredity. The present genetic theory has clearly failed to do that
(any book of developmental biology will prove that). The epigenetic theory of
heredity can show that mechanism in action in number of morphological and life
history characters (the development of mammary gland, production of egg cells,
development of blood vessels and, to a adequate degree in other developmental
processes such as formation of muscles, bones, regeneration, etc).
2. To present a discrete mechanism of the generation and deposition in the egg
cell of the epigenetic information (=maternal factors + gene imprinting). The
gene theory has failed. The epigenetic theory of heredity has shown how that
information is generated and how that information flows into the gametes.  
3. To show where the information for activation/inactivation of nonhousekeeping
genes comes from. As put by J. Maynard Smith (1998) "It is not enough to say
that different genes are switched on in different places, although it is true.
We also need to know how the local action of specific genes is brought about." 
The gene theory has clearly failed to do that in more than half a century since
the discovery of the chemical nature of the gene. The epigenetic theory of
heredity proves that all the information for activating/inactivating
nonhousekeeping genes is of neural origin. Related to this,
4. To show the material structure where the immense information for erecting
metazoan organisms. The gene theory has clearly failed to do that too
(depending on the species, the amount of genetic information in the whole
genome of metazoans, in the best case,  hardly would represent more than one
thousandth of information for building a metazoan organism). The epigenetic
theory of heredity shows where that structure is and what it consists of.

I am looking forward to answer all the possible questions that would arise from
the comparison of the genetic and epigenetic theories of heredity and any other
question that might arise in relation to the epigenetic theory of heredity.

Thank you,

Nelson R. Cabej
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