已有 2235 次阅读 2021-7-29 20:04 |系统分类:科普集锦


龙当时提出大胆假说认为,这是一种对x染色体失活的补偿效应。文章发表在Genome Research上。



Retroposed New Genes Out of the X in Drosophila

Esther Betrán,Kevin Thornton,and Manyuan Long1,2,3

1Department of Ecology and Evolution; 2Committee on Genetics, The University of Chicago, Chicago, Illinois 60637, USA

New genes that originated by various molecular mechanisms are an essential component in understanding theevolution of genetic systems. We investigated the pattern of origin of the genes created by retroposition inDrosophila. We surveyed the whole Drosophila melanogaster genome for such new retrogenes and experimentallyanalyzed their functionality and evolutionary process. These retrogenes, functional as revealed by the analysisof expression, substitution, and population genetics, show a surprisingly asymmetric pattern in their origin.There is a significant excess of retrogenes that originate from the X chromosome and retropose to autosomes;new genes retroposed from autosomes are scarce. Further, we found that most of these X-derived autosomalretrogenes had evolved a testis expression pattern. These observations may be explained by natural selection favoring those new retrogenes that moved to autosomes and avoided the spermatogenesis X inactivation, andsuggest the important role of genome position for the origin of new genes.

[The sequence data from this study have been submitted to GenBank under accession nos. AY150701–AY150797.The following individuals kindly provided reagents, samples, or unpublished information as indicated in thepaper: M.-L. Wu, F. Lemeunier, and P. Gibert.]


Extensive gene traffic on the mammalian X chromosome

J J Emerson 1, Henrik Kaessmann, Esther Betrán, Manyuan Long

Mammalian sex chromosomes have undergone profound changes since evolving from ancestral autosomes. By examining retroposed genes in the human and mouse genomes, we demonstrate that, during evolution, the mammalian X chromosome has generated and recruited a disproportionately high number of functional retroposed genes, whereas the autosomes experienced lower gene turnover. Most autosomal copies originating from X-linked genes exhibited testis-biased expression. Such export is incompatible with mutational bias and is likely driven by natural selection to attain male germline function. However, the excess recruitment is consistent with a combination of both natural selection and mutational bias.



RPL10L Is Required for Male Meiotic Division by Compensating for RPL10 during Meiotic Sex Chromosome Inactivation in Mice

Long Jiang7  Tao LiXingxia Zhang Beibei Zhang Changping Yu Yang Li Suixing Fan Xiaohua Jiang Teka Khan Qiaomei Hao Peng Xu Daita Nadano Mahmoud Huleihel Eitan Lunenfeld P. Jeremy Wang Yuanwei Zhang'

Correspondence information about the author Yuanwei Zhang


  • Rpl10l is essential for the transition from prophase to metaphase in male meiosis I

  • Rpl10l expression compensates for Rpl10 silencing resulting from MSCI

  • Ectopically expressed RPL10L can substitute for RPL10 in cultured somatic cells

  • Rpl10 transgenic expression restores spermatogenesis and fertility of Rpl10l−/− males


The mammalian sex chromosomes have undergone profound changes during their evolution from an ancestral pair of autosomes [ 1–4 ]. Specifically, the X chromosome has acquired a paradoxical sex-biased function by redistributing gene contents [ 5, 6 ] and has generated a disproportionately high number of retrogenes that are located on autosomes and exhibit male-biased expression patterns [ 6 ]. Several selection-based models have been proposed to explain this phenomenon, including a model of sexual antagonism driving X inactivation (SAXI) [ 6–8 ] and a compensatory mechanism based on meiotic sex chromosome inactivation (MSCI) [ 6, 8–11 ]. However, experimental evidence correlating the function of X-chromosome-derived autosomal retrogenes with evolutionary forces remains limited [ 12–17 ]. Here, we show that the deficiency of Rpl10l, a murine autosomal retrogene of Rpl10 with testis-specific expression, disturbs ribosome biogenesis in late-prophase spermatocytes and prohibits the transition from prophase into metaphase of the first meiotic division, resulting in male infertility. Rpl10l expression compensates for the lack of Rpl10, which exhibits a broad expression pattern but is subject to MSCI during spermatogenesis. Importantly, ectopic expression of RPL10L prevents the death of cultured RPL10-deficient somatic cells, and Rpl10l-promoter-driven transgenic expression of Rpl10 in spermatocytes restores spermatogenesis and fertility in Rpl10l-deficient mice. Our results demonstrate that Rpl10l plays an essential role during the meiotic stage of spermatogenesis by compensating for MSCI-mediated transcriptional silencing of Rpl10. These data provide direct evidence for the compensatory hypothesis and add novel insight into the evolution of X-chromosome-derived autosomal retrogenes and their role in male fertility.



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