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Transcript
BOLIVARIAN REPUBLIC OF VENEZUELA
UNIVERSIDAD DEL ZULIA
NEUROSCIENCES INSTITUTE
GENETICS OF COMMON HERITABLE DISORDERS IN VENEZUELA
RESEARCH TRAINING PROGRAM
PROFESSOR: GLADYS MAESTRE, M.D
RISING TO FIXATION
Final Essay
JOSELYN ROJAS QUINTERO, M.D
ID. 13.933.162
Maracaibo, December 2005
Rising to Fixation
A freshly duplicated selfish element is likely to be slightly deleterious because it
takes up space in the genome and also makes use of the cell’s transcription and
translation machinery for a function that not only does not contribute to the cell but
wastes energy as well. Explain in terms of selection and drift why, in spite of the
above consideration, the element can rise to fixation in the population.
By definition, a selfish gene works only for itself, using any mean necessary
for its survival in the next generations1. And by any mean, it includes the
destruction of other genes while it is inserted in the DNA, and, the unique ability to
multiply inside the genome so that the gene can have as many copies as it can.
This intrinsic replication machinery that selfish elements have facilitates their
fixation within the genome, even though, they might not even have a specific
function, or worse, they can have disadvantageous effects on the host’s survival.
The fixation of this type of genes depends mainly on two aspects: the selfish
capacity of its replication and the method of fixation.
The ability of the selfish gene to multiply within its host’s genome and to be
able to replicate in the free-genomes is what I call selfish capacity. Since all
mutations (good, trivial or bad) always occur in an individual’s germline, this gene
has to duplicate intra-genome to ensure its survival in this specific individual, but its
necessity to “colonize” non-selfish-elements genomes is what makes this
sequence so enigmatic. Given that we are diploid individuals, one haploid genome
is colonized and the other isn’t, so during the formation of the first 2 cells of the
zygote the gene has to virtually “jump” (almost infectiously) and introduce itself in
the non-colonized genome2 “conquering” it (intergenomic multiplication in the free
haploid DNA). This process is, of course, done in a non-mendelian fashion.
It’s clear that this kind of gene is a transposable sequence which has
intragenomic replication machinery, and it multiplies at a certain frequency. The
more it copies the higher the frequency of it in the next generation, although a
lower rate of multiplication doesn’t alter the spreading since the intergenomic
capacity of colonization is what keeps it in the future populations 2; the only thing
that will change is the number of copies in each individual’s genome. So a
“selfisher” gene would be one that has various copies inside the DNA of the host,
made at a high rate, and can colonize faster the zygote´s cells. Only it can ensure
its survival, and that is being quicker than the other transposable elements.
The tricky question is what happens if this gene lowers the fitness of the
individual who carries it? It would have to be a very disadvantageous trait – lethal
or sterility related – to eliminate the host (extinct the gene). If the gene only lowers
the fitness then is just a matter of “selecting” the method of fixation.
In this case the gene “takes up space in the genome” and “wastes energy”,
so apparently it doesn’t interfere strongly with the reproductive capacities. By
Darwin’s definition3 during natural selection only the fittest survive, being this the
one that has more reproductive capabilities, ensuring a good number of offprings
that will continue the species. In a genomic level, the “fit individual” is without a
doubt a quick selfish gene. Even if the gene lowers the fitness, the host will
continue to procreate (at least 1 offspring) that will carry the gene and its copies,
and since it doesn’t produce a contra productive phenotype trait, selection “lets it
pass”. This is true unless during the next generations, the copies alters genomic
sequences that regulate procreation, at this point, selection will eliminate it.
Based on Darwin’s observations, the population will reproduce in an infinite
matter, but, what happens if by chance a natural disaster or a plague occurs? The
population will be shortened and the ones who survive will be selected by chance
not selection. Let’s assume that the survivors have the selfish gene, and being in
this bottleneck situation they will multiply to increase the population number,
passing the gene to all their descendants. Hence, this gene was then fixated by a
genetic drift method.
Another drift way to fixate a gene is the so called “founder effect” where one
individual settles in a new small population genetically different from him. Since the
matting will be likely non-random in the course of the following generations the
gene will be passed along in a Mendelian fashion, until every genome has it
(frequency 1). But keep in mind that a non-selfish-element genome is the
playground of a quick selfish gene, so the new population genome colonization will
be “just a walk in the park” (so to speak). In other words, it seems that a “selfisher”
gene would be better fixated during genetic drift situations, although with a closer
look, a fast-multiplying self-replicating gene fits better the description of Darwin’s
key to survival.
To summarize, a selfish gene is a genomic sequence with self-replicating
properties that can be fixated into the genome, even if it offers no benefits to the
host or group of individuals. This kind of sequence can be fixated by natural
selection or genetic drift, always depending of its own replicating characteristics.
CITED REFERENCES
1. DAWKINS, R. 1976 The Selfish Gene. Oxford University Press, Oxford.
2. HICKEY, D. “Selfish DNA: a sexually tranbsmitted nuclear parasite”. Genetics
1982;101:519-53.
3. FLEMING C, GOODALL J. “Dangerous Darwin”. Public Understand Sci 2002;11:259-71.