"LYSENKO, VIEWS OF NATURE
AND SOCIETY -
REDUCTIONIST BIOLOGY AS A KHRUSCHEVITE
REVISIONIST WEAPON"
First published in pamphlet format in Toronto; September 1993.
(pp.151-168).
Continuing With:
Part 1: (section 4 in web edition)
WESTERN GENETICISTS ATTRACTED
TO INHERITANCE OF ACQUIRED CHARACTERISTICS
Though orthodox biology held strongly against the view
first put by Jean Baptiste Lamarck, regarding the possibility of an inheritance
of acquired characters, this possibility annoyingly kept re-surfacing.
Lamarck's simplistic view of this is presented above, and was put very
much in the shade by the advent of Darwinism. But as discussed, Darwin
was himself, somewhat equivocal about whether or not he belied in Inheritance
by Acquired Characters.
In general, the scientists in the West following Darwin
and the aggressive attacks by Bateson upon Inheritance of Acquired Characters,
were mainly conventional Mendelian based. Kammerer has been discussed above,
and the reception his experiments received. However, the theory of Inheritance
of Acquired Characters kept cropping up again.
"among the most publicised Lamarckian experiments of
the 1920's were those of Michael Guyer at the University of Wisconsin,
who had claimed that certain genes could be altered by immunological influences..
he reported (1924) that when antibodies to lens protein were given or induced
in a pregnant female rabbit, they had an effect on newborn rabbits, and
that this condition was heritable."
p.168. Sapp, J.
"There was also the celebrated experiment of Griffith
of the late 1920's who showed that live Pneumococcus of one strain acquired
some of the characteristics of dead bacteria of another strain when both
strains were injected into a live animal.. this phenomenon could be seen
as a means of identifying genetic material as nucleic acid. However it
could also be seen as a case of directed hereditary alterations since the
heredity of one strain of bacteria was transformed by exposure to a specific
environment.. killed bacteria.. even non-Lysenkoists viewed the phenomenon
as.. inheritance of acquired characteristics.. Darlington and Mather
said : " Thus at the molecular level we can.. produce a pseudo-Lamarckian
effect. We can control heredity from the outside and control it.. constructively."
Sapp. p.169.
These and many other inconvenient experiments had to be dealt
with. The easiest way of doing so, was to force them into the mould of
a purely Central Dogma framework:
"Nucleocentric geneticists such as H.J.Muller.. attempted
to dismiss cases of migratory plasmagenes such as Kappa and Sigma.. as
infection. L'Heritier, Sonneborn, Darlington, Lederberg, Ephrussi,
and others opposed this interpretation.. There was the classical case of
Euglena as investigated by Charlotte Ternitz.. When Euglena mesnili..
which normally contains about 100 chloroplasts, is put in the dark the
number of chloroplasts diminishes to about one or two after some
months. The effects of use and disuse are inherited. Moreover individuals
without plastids, which are able to reproduce, may be formed at a mitotic
division, though they grow slowly and have never been kept for many generations.
Kappa in paramecium responded to environmental influences in a similar
way."
J. Sapp. p.169.
So while E.B.Wilson was prepared to concede some role
for the cytoplasm in organisation (See above quote), the Morganists were
much more belligerent, dismissing the evidences for cytoplasmic inheritance
in favour of the Mechanisms of Mendelian Heredity (1915). They considered
Correns' work simply reflected disease vectors carried by the cytoplasm
and dismissed Bauer altogether (Sapp Ibid, p. 27).
Plasmagenes - similar in concept to those thought
to be present by Darwin were invoked for the contradictions that kept arising
:
"L'Heritier discovered the so called genoid, sigma
in the cytoplasm of Drosophila as.. known to be transmitted by the egg
as well as the sperm.. he demonstrated that the genoid could migrate from
the body cells to the germ cells which then pass it on to later generations.
Plasmagenes which could migrate from the soma to germs cells provided a
possible mechanism for the inheritance of acquired characteristics."
p.169 Sapp.
SONNEBORN, PARAMECIUM
AND THE INHERITANCE OF ACQUIRED CHARACTERS
In the USA, Sonneborn was a particularly important proponent
of the view that there was in certain cases inheritance of acquired characters.
"(Regarding) Antigens in paramecium.. by choosing appropriate
environmental conditions, Sonneborn.. demonstrated that in paramecium it
was possible to direct transformation to one particular antigenic type
among the 8 possible types.. Moreover when an immobilization antiserum
was used in high enough concentrations to kill paramecium, the transformed
organisms were shown to be completely resistant to this agent.. the transformation
responding to the environmental agent was considered to be adaptive.. Interpretations
included cytoplasmic inheritance, plasmagenes.. or a mechanism at the supramolecular
level involving cytoplasmic fields and cytologically visible cell structures..
Sonneborn wrote: ' The main feature of the antigen work is that specifiable
environmental conditions can force upon the cells specifically adapted
and directed responses which are thereafter inherited through the cytoplasm.'..
"
P.169-70, 179 J.Sapp.
Sonneborn was aware that this view, might be percieved as
having led him to an uncomfortably close relationship to the Lysenkoists,
especially since the Lysenko-ists started quoting his "scriptures". He
was therefore at pains to attack the Lysenkoists, on their biological interpretations,
and their "political" motivations, whilst at the same time continuing the
examination for defining the role of cytoplasmic determinants of heredity.
He pointed out that his own work was still in marked
contradiction to the Lysenkoists since they denied the existence of any
special substances of heredity (See Part 2).
But he agreed that his experiments confirmed that inheritance
of acquired characters could occur, but insisted that this was because
of localised heritable particles. Therefore, he argued, he was in contradiction
with, and antagonistic to Lysenkoism which had clearly stated that each
part of the cell was involved in inheritance (Sapp, Ibid p. 179).
David Nanney was a worker in Sonneborn's lab, who
diverged from Sonneborn in a way that denied the exclusive importance of
particulate genes whether they were located in the nucleus or the cytoplasm.
He developed the notion of a "steady state" homeostasis which comes
extremely close to the type of notion later proposed by Lysenko in his
definition of heredity. For Nanney:
"(In the steady state).. we envision a dynamic self perpetrating
organisation of a variety of molecular species which owes its specific
properties not to the characteristics of any one kind of molecule but to
the functional interrelationship of these molecular species."
Cited Sapp, p. 196.
For Lysenko, the equivalent phrase, in fact it was a key
formulation of the Lysenkoists - was as follows:
"Heredity is the property of a living body to require
definite conditions for its life, its development, and to respond definitely
to the influence of particular conditions."
p.484. Lysenko, Agrobiology, Moscow, 1954.
It is of course interesting that this line of biological
reasoning can be traced right back to Darwin :
"Inheritance must be looked at as merely a form of growth."
Charles Darwin,1868,p.404. Cited by Sapp, Ibid, p.3.
From this Nanney, drew a picture of heredity as a description
of:
"The more general capacity of living material to maintain
its individuality (specificity) during proliferation.. "Heredity" in this
sense is a type of homeostasis, similar to physiological homeostasis but
implying more, since it includes regulation during protoplasmic increase."
Cited, Sapp, Ibid, p. 199.
Thus Nanney insisted instead to search for "epigenetic"
(tomean more thatn simple hereditary pariculate mechanisms, which often
came to be a synonym for developmental mechanisms)) mechanisms
that could explain the "regulation of expression of genetic potential,
and differentiated these from truly genetic mechanisms." :
"A recognition of the existence of two types of systems,
and even the difficulties in distinguishing between them, may be useful
in avoiding confusion in discussing cytoplasmic inheritance, developmental
alterations, inheritance of acquired characters, mutations and genetic
information."
Cited Sapp, Ibid, p.20.
This paradigm would lead him to argue that the unexplained
phenomena in the literature could be resolved by a call to cellular
homeostasis:
"In an attempt to support the importance and generality
of a non-particulate physical basis of heredity, Nanney suggested a reinterpretation
of some cases of cytoplasmic heredity claimed to be due to "plasmagenes",
but for which he claimed a particulate basis had not been established.
These included the "barrage" phenomenon in Podospora, serotypes in Paramecium,
poky in Neurospora, and Plasmon characters described by Michaleis in Epilobium.."
Sapp. p. 199
Needless to say Nanney drew the fire of many who were now
intent in their science in establishing that there were indeed genes in
the cytoplasm.
These now included such as Ruth Sager in the USA and
J.L.Jinks in the UK.
But no one was able to give a fully explanatory thoery
either then, or indeed up to even very recently. as Sapp rightly points
out:
"The physical basis of many cases of non-Mendelian inheritance,
especially Plasmon characteristics in higher plants, those concerning male
sterility and other physiological properties, remains obscure to this day.."
Sapp, Ibid; p. 202.
CHANCE REVISITED
Having now laid some ground work to understand molecular
genetics, we should revisit the issue of Chance. This we had left at a
somewhat abstract and philosophical level (See above section-Go to table
ofcontents -Link at foot of page).
We can now apply a molecular understanding to various
experimental systems that examine this central issue.
But to recap, there is a basic assumption underlying
the insistence upon Chance mutations.
This is that the organism receives no cues from the
environment that can guide future mutations. If it happens and if it is
selected, then a mutation thrives.
It is in no way, a directed response to the environment.
In an article wonderfully entitled : "How the Slot
Machine led Biologists Astray", G.Z.Opadia-Kadima shows how the basic assumptions
of some early molecular biology work led to a "misreading " of the data.
The slot machine refers to how the original experiments
were motivated, by the inspiration that we related before - whereby Luria
recieved an insight, whilst watching the Faculty Club Slot machine!
Thus in 1943, Salvador Luria and Max Delbruck devised
an experiment designed to test at a molecular level, whether chance led
to mutations in Escherichia coli (E.Coli) a bacterium.
But as Opadia-Kadima puts it:
"It is now more than 40 years since Darwin triumphed
over Lamarckism.. Unlike our embattled sires, we are in a position to take
a relaxed view of the events that led to the triumph. Especially we can
perceive with a measure of clarity that crucial argument which was employed
to clinch the victory was, in fact a falsehood.. Luria and Delbruck had
taken away the very cornerstone upon which Lamarckism rested.. In short
the biologists belief in the creative power of chance soon came equalled
or surpassed the Christian belief in the creative power of God.. Chance
was credited with creative feats formerly attributed only to God, Allah
and Karma".
G.Z.Opadia-Kadima: "How the Slot Machine led Biologists
Astray", J.Theoret. Biol. 1987; 124: 127-135.
Luria and Delbruck had hypothesised, that if E.Coli had
never seen the Bacteriophage T1 (actually a viral infection of bacteria),
it should not develop resistance to this infection, unless the godess Chance
played her hand and offered a mutant that conferred selective advantage.
And very quickly they found that indeed E.Coli could
develop resistance without apparently having met it before. This
was to them, stunning and convicing proof positive of the Randomness of
mutation and variation. Moreover, Lederberg had shown that in a similar
fashion, bacteria could become resistant to streptomycin without meeting
it.
But, as Opadia-Kadima shows however, there are some problems
with the interpretation of these now classical experiments. The slot machines
in the intellectual ambience of the Faculty Club had led Luria to design
his experiment. But so often, the sums of money won by slot machine playing
is very small, and:
"Individual pay outs (ie individual wins) are like individual
favourable variations, never large, always small. Before a win is gained
an investment had to be made.. Those who appear to be favoured by chance..
in fact turn out to be losers in the long run."
Opadia-Kadima, Ibid, p. 130.
Theoretically, the deficiencies of the Luria experimental
model are discussed by Opadia-Kadima.
1. Indeed chance variation will allow an occasionally
lucky organism ("one organism in several millions") to mutate. But The
"price paid will be high". This is becasue in the absence of the drug,
there is a selective disadvantage to having the mutation:
"Therefore on the absence of the drug, the few organisms
which mutate back to the wild type, eventually drive the isoenzyme-producing
mutants into extinction. In fact this why after the use of the drug has
been halted for some years, the resistant organism become sensitive to
it once again. .. The preadaptive mutations which Luria, Delbruck and Lederberg
investigated happen to belong to a group that is invariably eliminated
under natural conditions."
Opadia-Kadima, Ibid, p.130-31.
2. There is a great distinction between the natural
conditions and the artificial conditions of the laboratory. Thus in the
lab, the selective pressures involved also include antibiotics, that kill
off 99.99% of organisms. Thus lab conditions, leads to the selection of
the less fit, rather than the more fit - as occurs in general
in natural conditions. But in addition, the lab conditions impose a very
severe and sudden change in environment, which in the natural circumstances
is more likely to be slower. If it is slower, there is a possibility of
effecting some degree of evolutionary change:
"The lab conditions kills off, or prevents the reproduction
of 99.99% of organisms in a single generation. The consequence being that
the genomes of the organisms are denied th time needed for making evolutionary
responses (postadaptive mutation).. Under natural conditions on the other
hand the selective regime is not necessarily lethal.. it mainly imposes
hardship-it causes organisms to experience a need. Even in those cases
where it is lethal, it kills off, or prevents the reproduction of, only
a limited proportion of organisms in any one generation. This means that
the genomes of sot organisms have ample time for making evolutionary responses.
In particular there is ample time for stepwise mutations, spread over several
generations."
Opadia-Kadima, Ibid, p.130-31.
3. Furthermore, most evolutionary responses require
mutations in more than one gene simultaneously. A so called regulator
gene as well as a structural gene ( See the sections on the views
of Barbara McClintlock and Richard Goldschmidt). The issue of chance then
becomes even more "chancy", the more complex the change required.
4. A critical flaw of the Lederberg and Luria experiments
was the lack of understanding of the dynamics of mutation. The various
mutations to phage and streptomycin resistance are expressed only later
and after the change in DNA sequence has occurred. Thus Cairns et al
conclude:
"The resistant mutants one isolates by spreading culture
on a selective plates are the result of events that must have occurred
many generations before one applies the selection that demonstrates their
existence. So these classical experiments could not have detected (and
certainly did not exclude) the existence of a non-random possibly product-oriented
form of mutation."
Cairns, John, Julie Overbaugh and Stephen Miller. "The
origin of Mutants", Nature, 1988, 335; 142-145.
Of course this critique is quite hypothetical. But there
is also empirical data to show that the Luria model is incorrect.
Firstly, Campbell performed experiments that utilised
the notions that there are two genes that need to be mutated for effective
changes:
"When E.Coli strains carrying a deletion of the gene
for B-Galactosidase are cultivated on medium that is lactose free, they
do not recover the ability to utilize the sugar. It does not matter how
many generations are cultured.. the favourable variation involved requires
at least two mutations events (one in a structural gene another in a regulatory
gene) the probability of it being acquired by chance is no higher than
1 in 1014."
Opadia-Kadima, Ibid, p. 131
But the bugs can be induced to deal with this, by critically
limiting the availability of nutrients. In other words, by starving
them, when they are "forced" to use whatever nutrients are around,
in this case lactose. Lactose is hydrolysed (ie broken down) only then.
Instead of the anthropomorphic term "forced", the preferred term is that
there has been a "genomic stress". This was shown by Campbell, and
his experiment of 1973 is cited by Opadia-Kadima.
"The inability of the deletion-mutants to regain by chance
the ability to utilise the sugar is.. underlined by what happens when the
culture medium contains lactose as well as another source of carbon. The
strains just keep thriving on the non-lactose component of the nutrient;
not a single revertant emerges- thereby indicating that the presence of
the sugar does not increase their mutation rate.. However when the non-lactose
component of the nutrient is virtually exhausted, all that changes. The
strains attempt to utilize lactose (molecules of which are absorbed). But
because there is no B-Galactosidase to split up the sugar, they experience
a need with regard to the enzyme.. inducing "genomic stress'.. that sets
in train two processes of non-random mutations, aimed at.. the ability
to hydrolyse lactose. In the first of these two processes, a structural
gene whose product could not previously, hydrolyse lactose undergoes mutation
so that the new product it codes for can. The second process involves the
regulatory mechanism of this same structural gene. For whereas previously
the mechanisms was insensitive to lactose, its mutated form responds to
the presence of the sugar by permitting the transcription of the new gene."
Opadia-Kadima, Ibid p.131-33.
In fact the Campbell experiment had not shown simply a regaining
of the ability to hydrolyse lactose through the same enzyme system. In
fact a completely new enzyme system different from the previous one (f
or B-galactosidase) had been evolved. In similar experiments, Hall and
Hartl (Genetics 1974;76: p.391) duplicated the experiments and showed
that this new enzyme production was regulated by lactose.
As Opadia-Kadima concludes:
"The fact that the new enzyme evolved in response to
starvation in the presence of lactose, suggest that E.Coli are equipped
with a mechanism for causing new enzymes to come into being when the need
arises."
Opadia-Kadima, Ibid, p. 134.
And in a striking recent illustration of this radical notion,
John Cairns and co-workers suggest that:
"Cells may have mechanisms for choosing which mutations
will occur."
Cairns, John, Julie Overbaugh and Stephen Miller.
"The origin of Mutants", Nature, 1988, 335; 142-145.
These workers working with the E.Coli and lactose system
further sharpen the interaction between and the bacterial genome and the
environment it is placed in. To examine this, the authors looked at features
of the E.Coli that are immediately expressed, and where:
"The selection pressures rewards mutants by letting them
multiply by allows all the other, non-mutant cells to survive so that they
can at least have the opportunity to perform directed mutations."
Cairns, John, Ibid.
So the authors first calculated the expected distributions
given various differing types of mutationary change - in two resulting
conditions.
Firstly under a true random condition (Growth
curve A), and second under conditions where bacteria are "directed"
towards a selection pressure (Growth Curve B).
They then compared these curves to what happens in reality.
This meant examinig the shape of the growth curves of
E.Coli variants Lac+ (meaning they have the enzyme to
hydrolyse lactose) and Lac- (meaning they do not have
the enzyme to hydrolyse lactose) strains grown in lactose free conditions.
They also managed to also identify a region in the uvrB-bio
region of the E.Coli chromosome that appears to control the mutations,
that allow the bacteria to use lactose.
They then showed that this genomic area of the chromosome
gives rise a growth curve of the B type. ie. a curve showing that the
bacteria were "directed" towards the selection pressure.
They then played with the genes and prevented them
from becoming turned on, unless the bacteria themsleves performed some
directed minor surgery on the genes.
They found that indeed, the bacteria was able when
appropriate, to perform the surgery on the genes even though they had been
fiddled with; and begin to feed on the lactose.
Again the growth curve seemed to be the Growth Curve
B. ie.where bacteria are "directed" towards a selection pressure.
In more technical terms they looked at a strain in which
a different part of the chromosome : araC (which is a positive regulatory
element controlling the arabinose operon) is placed upstream of the area
controlling lactose breakdown, but separated from it by a short segment
of Mu DNA that contains transcription terminating signals in a mutant strain
LacZ that cannot metabolise lactose. This organism can then read and become
LAC+ only if the organism deletes an intervening mu sequence,
in which case it can grow if arabinose is provided. This phenotype is LAC(ARA)+.
There is a delay in the appearance of LAC(ARA)+, and this delay
is the time during whihc the organism is dependent upon the presence of
lactose in order to grow.The authors comment that this is:
"Another example of the production of appropriate mutations
in response to selection ".
But these are all experiments with inserted genes and
manipulating the genome. The final experiment reported in the paper examines
more natural forms of selection pressure.
Here so called "Cryptic genes" were examined.There
are apparently, an "extensive armoury of cryptic genes that can be called
upon for the metabolism of unusual substrates" (ie food).
Various bugs can therefore grow on different sugars.
Exactly how the cryptic genes kick in to enable the bug
to do so varies, but this may involve movements of parts of genes (insertion
sequences), or changes in the DNA code of several base pairs.
For the growth of Lacz- E.Coli mutants upon
lactose a cryptic gene (ebgA) requires to be turned on. This in
turn needs two mutations one in the repressor (ebgR) and one on
a site in the gene coding for enzyme (ebgA) to make the enzyme that
will hydrolyse lactose.
Normally these mutations occur very rarely (less often
than 10-8) and neither by themselves will enable LACZ to use
lactose. But colonies of this strain will grow within two weeks. The authors
comment that :
"It is difficult to imagine how bacteria care able to
solve complex problems like these-and do so without, at the same time accumulating
a large number of neutral and deleterious mutations-unless they
have access to some reversible process of trial and error."
Nature, Ibid.
The authors then discuss their results in a very frank
and aware manner. They realise that they are shaking the Central Dogma
Tree:
"The main purpose of this paper is to show how insecure
is our belief in the spontaneity (randomness) of most mutations,
it seems to be a doctrine that has never been properly put to the test.
We describe here a few experiments and some circumstantial evidence suggesting
that bacteria can choose which mutations they should produce...
Is all variation essentially random, like thermal noise?
Can the genome of the individual cell profit by experience?
At its extremes it was an argument between reductionist
and romantics.. the early triumph of molecular biology strongly supported
the reductionists..
Curiously when we come to consider what mechanism might
be the basis for the forms of mutations described in this paper, we find
that the molecular biologist has, in the interim, deserted the reductionist.
Now almost anything seems possible in certain systems,
information freely flows back from RNA to DNA; genomic instability can
be switched on under conditions of stress, and switched off when the stress
is over; and instances exist where cells are able to generate extreme variability
in localized regions of their genome. The only major category of informational
transfer that has not been described is between proteins and their messenger
RNA's that made them. If a cell discovered how to make that connection,
it might be able to exercise some choice over which mutations to accept
and which to reject. This is the kind of versatility and adaptability that
we seem to be seeing in these experiments."
The authors go on to suggest that retroviruses with
reverse transcription might be the mechanism that could provide this "versatility
and adaptability."
This mechanism has also been proposed by Edward Steele.
THE CASE OF STEELE
The controversies have not of course ended. As recently
as the 1980's another rather visible attack was launched on orthodoxy,
that aimed to legitimise Inheritance of Acquired Characters in the Immune
system. Of course the immune system has to be highly adaptive and flexible.
Just like the question of developmment then, it has proven to be a "test
case" of the notions of inflexiblity underlying the Central Dogma.
The potential of the immune system for showing inheritance
of acquired characteristics was recently exploited in high mammals (rabbits)
by Steele and co-workers. They demonstrated that rabbits were able
to inherit idiotype ( antibody ) responses to foreign injected substances.
This caused a great deal of controversy and has certainly held up the career
of Steele.
"Steele forges a three fold union of Burnet's
theory of clonal selection, Temin's provirus theory, and his own
attack on the sanctity of the Weissmann germ line . From Burnet he gets
the idea that of somatic mutation leading to genetic diversity among the
cells of the body. Natural selection within the body then sees to it that
the body becomes populated by successful cells at the expense of unsuccessful
varieties.. From Temin he gets the idea of RNA viruses serving as intracellular
messengers, transcribing genes in one cell, carrying the information to
another cell and reverse templating it back into DNA in the second cell
using reverse transcriptase."
R.Dawkins. p.166. " The Extended Phenotype " Oxford 1982.
It is fair to say that the results of Steele and co-workers
have as yet not been duplicated by other laboratories despite intense effort.
It is therefore as yet unclear whether or not the validity of Steele's
interpretations are correct.
However it is noticeable that at least on this occasion,
in the concentrated fire that was levelled at Steele, a certain even handedness
entered the debate. This is in marked contrast to the way in which Jollos,
McClintlock, and Goldschmidt were treated (let alone Lysenko). It is a
conjecture of this author, that the rise of revisionism in the USSR, that
had destroyed socialism, made it much less politically urgent to discredit
such potentially dangerous notions.
Indeed a sense prevailed, that it was correct to say that
: "The Jury was out", instead of a shrill dogmatic interdiction. This pervades
the editorial columns, even when Steele is being upbraided for his tenacity
in claiming precedence for the exploitation of the notion of reverse transcriptase
as used by the retroviruses.
In summary:
many workers in the Western laboratories of genetics
have shown in lower organisms, the responses of Inheritance of Acquired
Characters. All these various data gradually have forced a reassessment
of the overall view of inheritance.
As a memorable title for
a recent article in the Lancet put it : "Lamarck refuses to lie down".
POST NEW SYNTHESIS : WHERE
TO ?
There have ben several corroborations of the McClintlockian
view that the genome is flexible.
These have been key to a view that the restrictive New
Synthesis needs radical modification, if not discarding. Both above, and
in part 2 below, we have highlighted some concerns about the New Synthesis.
Here, we will attempt to distil them into a codified alternative view.
Of course, we do not suggest that this alternative has been fully accepted.
But there appears to be at least, a growing awareness of some key limitations
of the New Synthesis.
PART 1 : CONCLUSION
The rather depressing state of affairs regarding the
inheritance of cytoplasmic factors, was summarised by Jink in 1963 :
"We must admit that we know almost nothing about the
action or mechanism of differences inherited in the cytoplasm."
Cited J.Sapp, p.203.
Though speaking about cytoplasmic inheritance, his words
applied well to the whole complexity of the interaction of the nuclear
and the cytoplasmic apparatuses. Orthodox geneticists in the West are still
resistant to accepting that their theories have problems for the overall
interpretation of the gene. As C.D.Darlington said in 1964, in an
address to the First Oxford Chromosome Conference:
"Thus all who are busy either with the structure of molecules
or with the appearance of organisms, regard the chromosome as doing what
various theories, such as the chemical theory of the chromosome and the
chromosome theory of heredity, require it to do. They find that it is doing
its job, smoothly and well - so smoothly and so well that they can take
it for granted; they can deduce its properties; they do not need to observe
them."
Keller; ibid; p.91.
The restrictive paradigm mindset of the diehard Mendelists,
has definitely obstructed the path of a fuller understanding of the complex
interaction between genome and environment. The obituary for Barbara McClintlock
in BioEssays (November 1992) puts it as follows:
"It is not yet possible for us to evaluate the full significance
of B.McClintlock's scientific accomplishments. It is widely recognised
that her work on transposable elements revolutionized our thinking about
genomic stability and genome reorganisation. The fluid genome has replaced
the Constant Genome. But her observations that cells can rapidly detect
the presence of broken chromosome and repair the breaks are still not well
known, and their implications for the cell biology of heredity and for
evolution has not yet been fully explored."
J.A.Shapiro : Barbara McClintlock. 1902-1992. Obituary.
Bioessays. Vol 14. No. 11. p. 791. Nov. 1992. Cambridge.
It should be clear from even this short account, that
there has been sharp resistance - even outside of Russia - to the "conventional
genetics."
Particularly sharp resistance was offered when conventional
genetics adopted a static view of the genome. The resistance has been particularly
offered by developmental biologists whose concerns are precisely with changes
in the organism. And from the above, it is clear that dissidents were treated
harshly. The names Kammerer, McClintlock, Goldschmidt and Jollos would
testify to this adequately.
Those that level their shrill
attacks, solely upon the Soviet Union for "Politicisation of Science" during
this historical period, will we hope look to their own glass houses.
Of course conventional genetics has
been wildly successful.
But it can only be foolish to deny that its emphasis
on a narrow focus has been a disservice to the further development of biology.
The relevance of this to the history of Lysenkoism will
be made clear in the next section.