Journal
DEVELOPMENT
Volume 146, Issue 4, Pages -Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.174037
Keywords
USP22; SAGA; Placenta; Vascular development; TGF beta signaling; RTK receptors; Endothelial cells; Pericytes; Mouse
Categories
Funding
- National Institutes of Health [R01GM096472, R01HD094400]
- Cancer Prevention Research Institute of Texas Training Program [RP170067]
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USP22, a component of the SAGA complex, is overexpressed in highly aggressive cancers, but the normal functions of this deubiquitinase are not well defined. We determined that loss of USP22 in mice results in embryonic lethality due to defects in extra-embryonic placental tissues and failure to establish proper vascular interactions with the maternal circulatory system. These phenotypes arise from abnormal gene expression patterns that reflect defective kinase signaling, including TGF beta and several receptor tyrosine kinase pathways. USP22 deletion in endothelial cells and pericytes that are induced from embryonic stem cells also hinders these signaling cascades, with detrimental effects on cell survival and differentiation as well as on the ability to form vessels. Our findings provide new insights into the functions of USP22 during development that may offer clues to its role in disease states.
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