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      Genomic imprinting mediates dosage compensation in a young plant XY system

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          Y-chromosome evolution: emerging insights into processes of Y-chromosome degeneration.

          The human Y chromosome is intriguing not only because it harbours the master-switch gene that determines gender but also because of its unusual evolutionary history. The Y chromosome evolved from an autosome, and its evolution has been characterized by massive gene decay. Recent whole-genome and transcriptome analyses of Y chromosomes in humans and other primates, in Drosophila species and in plants have shed light on the current gene content of the Y chromosome, its origins and its long-term fate. Furthermore, comparative analysis of young and old Y chromosomes has given further insights into the evolutionary and molecular forces triggering Y-chromosome degeneration and into the evolutionary destiny of the Y chromosome.
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            Sex Chromosomes and Sex-Linked Genes

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              The evolution of chromosomal sex determination and dosage compensation.

              In many species, sex is determined by a system based on X and Y chromosomes, the latter having lost much of their genetic activity. Y chromosomes have evolved independently many times, and the associated change in gene dosage in the heterogametic (XY) sex is often compensated for by regulatory mechanisms which ensure equal amounts of gene products of X-linked loci in males and females. There have recently been substantial advances in our knowledge of the molecular biology and genetics of sex chromosomes and dosage compensation, and in our understanding of the population genetic processes which are involved in their evolution.
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                Author and article information

                Journal
                Nature Plants
                Nature Plants
                Springer Nature America, Inc
                2055-0278
                August 13 2018
                Article
                10.1038/s41477-018-0221-y
                30104649
                4bb1fd11-d126-499d-b502-09e0d5fde796
                © 2018

                http://www.springer.com/tdm

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