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Dual role of PpV in Drosophila crystal cell proliferation and survival
Wang Luo1,2,† , Fang Zhang1,2,† , Fangzhen Zhao1,2 , Yang Fang1,2 , Long Zhao1,3,* , Ying Su1,2,*
1Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity, Ocean University of China, Qingdao 266003, China
2College of Marine Life Sciences, Ocean University of China, Qingdao 266003, China
3Fisheries College, Ocean University of China, Qingdao 266003, China
These authors contributed equally to this work
*Correspondence to:Ying Su , Email:suying@ouc.edu.cn Long Zhao , Email:zhaolong@ouc.edu.cn
J Mol Cell Biol, Volume 16, Issue 9, September 2024, mjae028,  https://doi.org/10.1093/jmcb/mjae028
Keyword: protein phosphatase, blood cells, Notch pathway, lymph gland, mechanical injury

Drosophila melanogaster crystal cells are a specialized type of blood cells for the innate immune process upon injury. Under normal conditions, crystal cells rarely proliferate and constitute a small proportion of fly blood cells. Notch signaling has been known to guide the cell fate determination of crystal cells and maintain their survival. Here, we reported that protein phosphatase V (PpV), the unique catalytic subunit of protein phosphatase 6 in Drosophila, is a novel regulator of crystal cell proliferation and integrity. We found that PpV proteins highly accumulated in crystal cells in the larval hematopoietic organ termed the lymph gland. Silencing PpV using RNA interference led to increased crystal cell proliferation in a Notch-independent manner and induced crystal cell rupture dependent on Notch signaling. Moreover, additive PpV prevented the rupture of crystal cells in lymph glands upon a needle injury, suggesting the involvement of PpV in wound healing. Altogether, our results indicated that PpV plays a dual role in lymph glands, preventing crystal cell proliferation to limit the cell number, as well as inhibiting crystal cell rupture to maintain their survival.