期刊
DEVELOPMENTAL CELL
卷 40, 期 3, 页码 289-301出版社
CELL PRESS
DOI: 10.1016/j.devcel.2016.12.023
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资金
- Francis Crick Institute from Cancer Research UK
- UK Medical Research Council [U117588498]
- Wellcome Trust
- NIHR Clinical Lectureship
- Academy of Medical Sciences grant [AMS-SGCL5]
- Academy of Medical Sciences (AMS) [AMS-SGCL5-Sangrithi] Funding Source: researchfish
- Medical Research Council [MC_U117588498] Funding Source: researchfish
- National Institute for Health Research [CL-2010-18-003, ACF-2007-18-013] Funding Source: researchfish
- The Francis Crick Institute [10415, 10193] Funding Source: researchfish
- MRC [MC_U117588498] Funding Source: UKRI
Somatic X dosage compensation requires two mechanisms: X inactivation balances X gene output between males (XY) and females (XX), while X upregulation, hypothesized by Ohno and documented in vivo, balances X gene with autosomal gene output. Whether X dosage compensation occurs in germ cells is unclear. We show that mouse and human germ cells exhibit non-canonical X dosage states that differ from the soma and between the sexes. Prior to genome-wide reprogramming, X upregulation is present, consistent with Ohno's hypothesis. Subsequently, however, it is erased. In females, erasure follows loss of X inactivation, causing X dosage excess. Conversely, in males, erasure leads to permanent X dosage decompensation. Sex chromosomally abnormal models exhibit a sex-reversed X dosage state: XX males, like XX females, develop X dosage excess, while XO females, like XY males, develop X dosage decompensation. Thus, germline X dosage compensation states are determined by X chromosome number, not phenotypic sex. These unexpected differences in X dosage compensation states between germline and soma offer unique perspectives on sex chromosome infertility.
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