The regulatory relationship between RagA and Nprl2 in <i>Drosophila</i> gut development.

Chunmei Niu; Jianwen Guan; Guoqiang Meng; Ying Zhou; Youheng Wei

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The regulatory relationship between RagA and Nprl2 in Drosophila gut development.

Author: Chunmei NIU ¹ ; Jianwen GUAN ¹ ; Guoqiang MENG ¹ ; Ying ZHOU ¹ ; Youheng WEI ¹
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1. College of Biological Science and Technology, Yangzhou University, Yangzhou 225000, Jiangsu, China.
Publication Type:Journal Article
Keywords: Drosophila; RagA; development; intestinal; nprl2 mutant
MeSH: Animals; Drosophila/genetics*; Mechanistic Target of Rapamycin Complex 1/metabolism*; Mammals/metabolism*; Carrier Proteins; Tumor Suppressor Proteins/metabolism*; Drosophila Proteins/genetics*
From: Chinese Journal of Biotechnology 2023;39(4):1747-1758
CountryChina
Language:Chinese
Abstract: The gastrointestinal tract is the largest digestive organ and the largest immune organ and detoxification organ, which is vital to the health of the body. Drosophila is a classic model organism, and its gut is highly similar to mammalian gut in terms of cell composition and genetic regulation, therefore can be used as a good model for studying gut development. target of rapmaycin complex 1 (TORC1) is a key factor regulating cellular metabolism. Nprl2 inhibits TORC1 activity by reducing Rag GTPase activity. Previous studies have found that nprl2 mutated Drosophila showed aging-related phenotypes such as enlarged foregastric and reduced lifespan, which were caused by over-activation of TORC1. In order to explore the role of Rag GTPase in the developmental defects of the gut of nprl2 mutated Drosophila, we used genetic hybridization combined with immunofluorescence to study the intestinal morphology and intestinal cell composition of RagA knockdown and nprl2 mutated Drosophila. The results showed that RagA knockdown alone could induce intestinal thickening and forestomach enlargement, suggesting that RagA also plays an important role in intestinal development. Knockdown of RagA rescued the phenotype of intestinal thinning and decreased secretory cells in nprl2 mutants, suggesting that Nprl2 may regulate the differentiation and morphology of intestinal cells by acting on RagA. Knockdown of RagA did not rescue the enlarged forestomach phenotype in nprl2 mutants, suggesting that Nprl2 may regulate forestomach development and intestinal digestive function through a mechanism independent of Rag GTPase.