I chose M. Sc. over MBA because I was interested in sex (evolution!!!!!). During my master, it always puzzled me why there is X-chromosome inactivation in female. It left an impression in my mind that inactivation of X-chromosome is a universal mechanism for dosage compensation in species that have two X-chromosomes in one sex. It taught me that nature want to equalize male and female. But this idea got changed last week when I came to know that Drosophila has different mechanism for the dosage compensation. It occurs in male Drosophila instead of female. The X chromosome is specifically targeted by male specific lethal (MSL)-complex that increases the transcription of X-linked genes by two-fold. MSL-complex is absent in female. This forced me to think that even evolution is biased for male in human. The first simple logic is that the ratio of expression of Y-linked genes to X-linked genes in human and Drosophila. Since Drosophila has two fold increment for X-linked genes, the ratio is ½ in male fly whereas it is just 1/1 in human male. The Y chromosome contains genes related to masculinity whereas X-chromosome contains genes for feminity. So nature favors more expression of female related genes in lower organism than human. Is this the really reason that human have the X-chromosome inactivation in female than two- fold increment in male like fly. The second reason could be cancer (it came in my mind because my father died due to cancer). It might be that X-chromosome contains proto-oncogenes. I found that one proto-oncogene (ARAF1) of 98 oncogenes is on  X-chromosome in human. This looks simple and straightforward that to control the expression of the ARAF1 below the threshold level, nature opted for the X-chromosome inactivation than two-fold increment of X-linked genes in male. This might be true if there is no other oncogene on X-chromosome but we cannot tell confidently. Moreover, it is puzzling to me that why nature selects the ARAF1 on X-chromosome than autosome. Will the ARAF1 not be active on autosome?  Will it be more frequently oncogenic when resides on autosome than X-chromosome? Therefore, I think that there are more uncharacterized oncogenic genes on X-chromosome or the chance of converting oncogene from proto-oncogene is less when the gene is regulated on X-chromosome (seems odd due to lack of recombination between sex chromosomes, there is more chance of accumulation of mutation on X-chromosme). Whatever the reason, but it also suggests that nature wants to protect male from cancer due to higher expression of oncogenes on X-chromosome.

Therefore, it looks to me that nature is gender bias at least in the case of human. I have been reading many articles that nature favors X-chromosome as there is disintegration of Y-chromosome, people predict that this erosion might cause complete loss of Y-chromosome and genes related to masculinity. Now, I think just reverse of this that nature selected X-chromosome for oncogenes and make Y-chromosome free of oncogenes. In other words, there are no oncogenes on Y-chromosome but there is at least one oncogene in X-chromosome, which makes X-chromosome oncogenic.It will be interesting to test in lower organism for enrichment of cell division genes on sex chromosome or on the mating type chromosome.

One of the hypotheses of sex chromosome evolution is lack of recombination between two homologous chromosomes. Lack of recombination causes accumulation of mutations, which is coupled with dosage compensation on X-chromosome and disintegration of Y-chromosome linked genes. Therefore, people believe that lack of crossing over leads the evolution of sex chromosome. Further, differentiation of sex chromosome from homologous pair of autosome select dosage compensation machinery. Identification of binding site of MSL complex in D. Miranda would be useful to test whether increasing of expression of genes by two-fold on one autosome will lead to the evolution of sex chromosome from this autosomes. This would tell whether dosage compensation is coupled with sex chromosome evolution as the lack of recombination is.  The other hypothesis that disintegration of Y-chromosome linked genes causes dosages compensation is not true at least in Drosophila.

Finally, It still left me thinking whether evolution of cancer genes is coupled with sex evolution. Thus, understanding sex chromosomes are always more fascinating than understanding the opposite sex.