One of the books I am reading right now is Austin Burt and Robert Triver's(2006) Genes in Conflict from Harvard University Press. An outline of the chapters is here. The basic premise of the book is that genes in an organism don't always agree and may spread even though the individuals bearing the genes may have reduced reproductive success. So these genes are a type of selfish genetic element which Burt and Trivers more precisely define as
"...stretches of DNA (genes, fragments of genes, noncoding DNA, portions of chromosomes, whole chromosomes, or sets of chromosomes) that act narrowly to advance their own interests-in other words, replication at the expense of the larger organism." p 2.
This notion is not entirely new. After all, early on in the 20th century geneticists discovered meiotic drive where genes or chromosomes can spread by distorting the 1:1 segregation ratios expected during meiosis. So for instance if you have an individual who is heterozygous Aa, we expect that half the gametes will have the A allele and half the a allele. But in meiotic drive this segregation ration is distorted and this bias can cause the spread of the allele biased for by meiotic drive even if the over all Darwinian fitness of the individual is reduced.
In what may seem contradictory, Burt and Triver's work is an extension of W.D. Hamilton's work on kin selection in which a a gene that reduces an individual's reproductive success (classical Darwinian fitness) may spread if the individual bearing the gene, increases the reproductive success of kin. This can work of course since kin are more likely to have copies of the gene. Much of Triver's work early on was in the area of genetic conflict vs cooperation among interacting organisms say parent offspring or even between interacting species as in the notion of reciprocal altruism.
I like Burt and Triver's book because you don't have to read it straight through and I often dip into it for good examples of how genes act...and these are relatively independent of whether or not you have read the rest of the book. The other nice thing about the book is that it integrates population thinking with molecular genetics in a very natural way, so that molecularly oriented biologists will hopefully begin to think about how these systems arise and behave in an evolutionary framework. On the other hand more classically trained population genetics types will begin to think less simply about the mechanisms involved in the systems we try to model at the population level. Also Burt and Trivers are careful to point out when information is lacking either at the molecular or at the evolutionary level.
Without going through the whole book here are a couple variations on the selfish genetic elements covered by Burt and Trivers. First are selfish sex chromosomes. For instance while in mammals males are usually XY and females XX, in some rodents there are 'feminizing' X and 'feminizing' Y chromosomes (denoted X* and Y*) In those rodent species with feminizing X* chromosomes along with regular X chromosomes there are three types of females possible XX , X*X, and X*Y and only one type of male XY. Notice that when the X*Y female mates you end up with the following situation:
1/4 of the zygotes will be X*X (female), 1/4 will be X*Y (female), 1/4 XY(male) and 1/4 YY. The YY individuals are not viable so that means the X*Y females have reduced individual fitness. Yet even in the simplest situation the X* chromosome can spread until it becomes so common that individuals with the X chromosome out produce them.
Another variation of on the theme of selfish genetic elements is genetic imprinting. In genetic imprinting the expression of a gene is dependent on which parent the gene is from. Classically for instance the phenotype of a heterozygote (Aa) is not affected by which parent donates the two alleles. In mice a gene called Igf2 is only expressed if inherited from the father. If this gene is inherited from the mother it is not expressed or maternally imprinted. There is no change in the nucleotide sequence in these imprinted genes, but the some of the nucleotide bases are methylated in the imprinted genes. One interesting thing about imprinting is that the the imprinted status of a gene is reversed from one generation to the next in the germline. First, the DNA methylation is removed and then the sex appropriate imprinting is done. So for instance for Igf2, the imprinted copy of this gene inherited by a female mouse from the father will not be expressed. But in her germ cells, the methylation is undone and that unimprinted gene is passed on to her offspring! Conversely for a male mouse the unimprinted copy of the gene from his mother is methylated in his germline cells.
Clearly this sort of regular system must have an evolutionary origin and Burt and Trivers nicely review the hypotheses about the origin of this system. Their thesis and the thrust of other researchers in this area is that imprinting arises because of a conflict between genes of maternal origin versus those of paternal origin. This conflict may be played out in the way different genes affect investment in the fetus and fetal growth rates. To see why consider a mother who mates with only one male in her life. There should be no conflict between these parents over how much parental investment to make in the offspring, since both parents loose equally say if the offspring uses to many resources during development.
But suppose the female mates with more than one male in her life or all the offspring are sired by different males. Then those males who pass on genes that increase the growth rate of their fetus at the expense of those of other males would have the advantage, even if this rapid fetal growth rate harms the mother to some degree. The mother on the other hand would benefit most by suppressing (imprinting) those genes that are paternally active and activating genes that benefit her interests. Probably the best way to say this is that the parents have a conflict over which sets of genes tied to development best serves each parent's interest.
Burt and Trivers view it as no accident that most of the 100 or so genes (out or 30,000 in the human genome) that are imprinted are fetal growth related. For instance the Igf2 gene is paternally active(maternally imprinted) and it increases size at birth by about 40%. The Igf2r gene in mice is maternally active(paternally imprinted) and it has the affect of decreasing size at birth. So these genes are acting in opposite ways and tend to cancel each other out in terms of net effects, exactly according to Burt and Trivers, what would be expected to be the evolutionary result of a conflict between maternal and paternal interests.
If your head is spinning, welcome to the club. Probably the best statement of what Burt and Trivers are getting at here is in the very last paragraph in the book:
"The unity of the organism is an approximation, undermined by these continuously emerging selfish elements with their alternative, narrowly self-benefiting means for boosting transmission to the next generation. The result: a parallel universe of (often intense) sociogenetic interactions within the individual organism-a world that evolves according to its own rules, as modulated by the sexual and social loves of the hosts and the Mendelian system that acts in part to suppress them."
So yes, cooperation is important in evolution but even within the individual organism genes don't act in a united fashion, for rogue genetic elements favoring one interest over another are constantly arising and at a very basic level the individual organism and it's genetics are shaped by this fact.
A further discussion of Triver's work by Razib at Gene Expressions.
Interview with Trivers on Edge.
Robert Trivers' Homepage.
Austin Burt's Homepage.
Theory of Genomic Imprinting in Insects.
week of science