Abstract
Two isoforms of the human ribosomal protein S4 gene,RPS4XandRPS4Y,are located on the X and Y chromosomes. It has been postulated that haploinsufficiency of these genes may contribute to Turner syndrome. We show here that several animal species that show the Turner-like phenotype on monosomy X have no Y-linkedRps4homolog. There may be another gene(s) that contributes to abnormal phenotypes of monosomy X. Molecular evolutionary analysis shows that the Y-linked andRPS4X-related homologs diverged prior to the radiation of placental mammals and evolved independently. Furthermore, the functional constraints against theRPS4X-related homologs are much stronger than those against the Y-linked homologs.
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