USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta

Evangelia Koutelou; Li Wang; Andria C. Schibler; Hsueh Ping Chao; Xianghong Kuang; Kevin Lin; Yue Lu; Jianjun Shen; Collene R. Jeter; Andrew Salinger; Marenda Wilson; Yi Chun Chen; Boyko S. Atanassov; Dean G. Tang; Sharon Y.R. Dent

doi:10.1242/dev.174037

USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta

Evangelia Koutelou, Li Wang, Andria C. Schibler, Hsueh Ping Chao, Xianghong Kuang, Kevin Lin, Yue Lu, Jianjun Shen, Collene R. Jeter, Andrew Salinger, Marenda Wilson, Yi Chun Chen, Boyko S. Atanassov, Dean G. Tang, Sharon Y.R. Dent

Epigenetics & Molecular Carcinogenesis

Research output: Contribution to journal › Article › peer-review

28 Scopus citations

Abstract

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 TGFβ 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.

Original language	English (US)
Article number	dev174037
Journal	Development (Cambridge)
Volume	146
Issue number	4
DOIs	https://doi.org/10.1242/dev.174037
State	Published - Feb 2019

Keywords

Endothelial cells
Mouse
Pericytes
Placenta
RTK receptors
SAGA
TGFβ signaling
USP22
Vascular development

ASJC Scopus subject areas

Molecular Biology
Developmental Biology

MD Anderson CCSG core facilities

Genetically Engineered Mouse Facility
Research Animal Support Facility
Science Park Flow Cytometry

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10.1242/dev.174037

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Koutelou, E., Wang, L., Schibler, A. C., Chao, H. P., Kuang, X., Lin, K., Lu, Y., Shen, J., Jeter, C. R., Salinger, A., Wilson, M., Chen, Y. C., Atanassov, B. S., Tang, D. G., & Dent, S. Y. R. (2019). USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta. Development (Cambridge), 146(4), Article dev174037. https://doi.org/10.1242/dev.174037

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title = "USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta",

abstract = "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 TGFβ 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.",

keywords = "Endothelial cells, Mouse, Pericytes, Placenta, RTK receptors, SAGA, TGFβ signaling, USP22, Vascular development",

author = "Evangelia Koutelou and Li Wang and Schibler, {Andria C.} and Chao, {Hsueh Ping} and Xianghong Kuang and Kevin Lin and Yue Lu and Jianjun Shen and Jeter, {Collene R.} and Andrew Salinger and Marenda Wilson and Chen, {Yi Chun} and Atanassov, {Boyko S.} and Tang, {Dean G.} and Dent, {Sharon Y.R.}",

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year = "2019",

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doi = "10.1242/dev.174037",

language = "English (US)",

volume = "146",

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AU - Koutelou, Evangelia

AU - Wang, Li

AU - Schibler, Andria C.

AU - Chao, Hsueh Ping

AU - Kuang, Xianghong

AU - Lin, Kevin

AU - Lu, Yue

AU - Shen, Jianjun

AU - Jeter, Collene R.

AU - Salinger, Andrew

AU - Wilson, Marenda

AU - Chen, Yi Chun

AU - Atanassov, Boyko S.

AU - Tang, Dean G.

AU - Dent, Sharon Y.R.

PY - 2019/2

Y1 - 2019/2

N2 - 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 TGFβ 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.

AB - 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 TGFβ 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.

KW - Endothelial cells

KW - Mouse

KW - Pericytes

KW - Placenta

KW - RTK receptors

KW - SAGA

KW - TGFβ signaling

KW - USP22

KW - Vascular development

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USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta

Abstract

Keywords

ASJC Scopus subject areas

MD Anderson CCSG core facilities

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