Mammalian Y chromosomes retain widely expressed dosage-sensitive regulators

Daniel W. Bellott (), Jennifer F. Hughes, Helen Skaletsky, Laura G. Brown, Tatyana Pyntikova, Ting-Jan Cho, Natalia Koutseva, Sara Zaghlul, Tina Graves, Susie Rock, Colin Kremitzki, Robert S. Fulton, Shannon Dugan, Yan Ding, Donna Morton, Ziad Khan, Lora Lewis, Christian Buhay, Qiaoyan Wang, Jennifer Watt, Michael Holder, Sandy Lee, Lynne Nazareth, Jessica Alföldi, Steve Rozen, Donna M. Muzny, Wesley C. Warren, Richard A. Gibbs, Richard K. Wilson and David C. Page
Additional contact information
Daniel W. Bellott: Whitehead Institute, Howard Hughes Medical Institute, Massachusetts Institute of Technology
Jennifer F. Hughes: Whitehead Institute, Howard Hughes Medical Institute, Massachusetts Institute of Technology
Helen Skaletsky: Whitehead Institute, Howard Hughes Medical Institute, Massachusetts Institute of Technology
Laura G. Brown: Whitehead Institute, Howard Hughes Medical Institute, Massachusetts Institute of Technology
Tatyana Pyntikova: Whitehead Institute, Howard Hughes Medical Institute, Massachusetts Institute of Technology
Ting-Jan Cho: Whitehead Institute, Howard Hughes Medical Institute, Massachusetts Institute of Technology
Natalia Koutseva: Whitehead Institute, Howard Hughes Medical Institute, Massachusetts Institute of Technology
Sara Zaghlul: Whitehead Institute, Howard Hughes Medical Institute, Massachusetts Institute of Technology
Tina Graves: The Genome Institute, Washington University School of Medicine
Susie Rock: The Genome Institute, Washington University School of Medicine
Colin Kremitzki: The Genome Institute, Washington University School of Medicine
Robert S. Fulton: The Genome Institute, Washington University School of Medicine
Shannon Dugan: Human Genome Sequencing Center, Baylor College of Medicine
Yan Ding: Human Genome Sequencing Center, Baylor College of Medicine
Donna Morton: Human Genome Sequencing Center, Baylor College of Medicine
Ziad Khan: Human Genome Sequencing Center, Baylor College of Medicine
Lora Lewis: Human Genome Sequencing Center, Baylor College of Medicine
Christian Buhay: Human Genome Sequencing Center, Baylor College of Medicine
Qiaoyan Wang: Human Genome Sequencing Center, Baylor College of Medicine
Jennifer Watt: Human Genome Sequencing Center, Baylor College of Medicine
Michael Holder: Human Genome Sequencing Center, Baylor College of Medicine
Sandy Lee: Human Genome Sequencing Center, Baylor College of Medicine
Lynne Nazareth: Human Genome Sequencing Center, Baylor College of Medicine
Jessica Alföldi: Whitehead Institute, Howard Hughes Medical Institute, Massachusetts Institute of Technology
Steve Rozen: Whitehead Institute, Howard Hughes Medical Institute, Massachusetts Institute of Technology
Donna M. Muzny: Human Genome Sequencing Center, Baylor College of Medicine
Wesley C. Warren: The Genome Institute, Washington University School of Medicine
Richard A. Gibbs: Human Genome Sequencing Center, Baylor College of Medicine
Richard K. Wilson: The Genome Institute, Washington University School of Medicine
David C. Page: Whitehead Institute, Howard Hughes Medical Institute, Massachusetts Institute of Technology

Nature, 2014, vol. 508, issue 7497, 494-499

Abstract: Abstract The human X and Y chromosomes evolved from an ordinary pair of autosomes, but millions of years ago genetic decay ravaged the Y chromosome, and only three per cent of its ancestral genes survived. We reconstructed the evolution of the Y chromosome across eight mammals to identify biases in gene content and the selective pressures that preserved the surviving ancestral genes. Our findings indicate that survival was nonrandom, and in two cases, convergent across placental and marsupial mammals. We conclude that the gene content of the Y chromosome became specialized through selection to maintain the ancestral dosage of homologous X–Y gene pairs that function as broadly expressed regulators of transcription, translation and protein stability. We propose that beyond its roles in testis determination and spermatogenesis, the Y chromosome is essential for male viability, and has unappreciated roles in Turner’s syndrome and in phenotypic differences between the sexes in health and disease.

Date: 2014
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DOI: 10.1038/nature13206

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