| First Author | Sangrithi MN | Year | 2017 |
| Journal | Dev Cell | Volume | 40 |
| Issue | 3 | Pages | 289-301.e3 |
| PubMed ID | 28132849 | Mgi Jnum | J:356039 |
| Mgi Id | MGI:7762131 | Doi | 10.1016/j.devcel.2016.12.023 |
| Citation | Sangrithi MN, et al. (2017) Non-Canonical and Sexually Dimorphic X Dosage Compensation States in the Mouse and Human Germline. Dev Cell 40(3):289-301.e3 |
| abstractText | 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. |
