한빛사논문
- 조회396
Bumsik Cho,1,2 Mingyu Shin,1 Eunji Chang,1 Seogho Son,1 Incheol Shin,1,2,3 and Jiwon Shim 1,2,3,4,5,*
1Department of Life Science, College of Natural Science, Hanyang University, Seoul 04763, Republic of Korea
2Research Institute for Natural Science, Hanyang University, Seoul 04763, Republic of Korea
3Research Institute for Convergence of Basic Science, Hanyang University, Seoul 04763, Republic of Korea
4Hanyang Institute of Bioscience and Biotechnology, Hanyang University, Seoul 04763, Republic of Korea
5Lead contact
*Corresponding author: correspondence to Jiwon Shim
Abstract
The Drosophila lymph gland houses blood progenitors that give rise to myeloid-like blood cells. Initially, blood progenitors proliferate, but later, they become quiescent to maintain multipotency before differentiation. Despite the identification of various factors involved in multipotency maintenance, the cellular mechanism controlling blood progenitor quiescence remains elusive. Here, we identify the expression of nitric oxide synthase in blood progenitors, generating nitric oxide for post-translational S-nitrosylation of protein cysteine residues. S-nitrosylation activates the Ire1-Xbp1-mediated unfolded protein response, leading to G2 cell-cycle arrest. Specifically, we identify the epidermal growth factor receptor as a target of S-nitrosylation, resulting in its retention within the endoplasmic reticulum and blockade of its receptor function. Overall, our findings highlight developmentally programmed S-nitrosylation as a critical mechanism that induces protein quality control in blood progenitors, maintaining their undifferentiated state by inhibiting cell-cycle progression and rendering them unresponsive to paracrine factors.
논문정보
- Research article
- 2024년 03월 (BRIC 등록일 2024-03-25)
- 국내 연구진
- 생명과학 > 발생생물학
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