Pss knockdown in the midgut causes growth retardation in Drosophila similar to that in human LMHD.

IF 1.5 3区生物学 Q2 ANATOMY & MORPHOLOGY

Developmental Dynamics Pub Date : 2025-05-22 DOI:10.1002/dvdy.70039

Kwan-Young Kim, You-Lim Hwang, Sunwoo Yeom, Seung-Hae Kwon, Sang-Hak Jeon

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引用次数: 0

Abstract

Background: Phosphatidylserine synthase (PSS), localized in the mitochondrial membrane, synthesizes phosphatidylserine. In humans, mutations in Pss lead to Lenz-Majewski hyperostotic dwarfism, a disorder affecting growth and development. The effects of Pss mutations on the growth of Drosophila melanogaster are not fully known. Hence, this study was conducted to investigate the effects of Pss knockdown on the growth and development of D. melanogaster.

Results: Enterocyte (EC)-specific Pss knockdown resulted in reduced cell size in the gut via reduced Akt signaling. EC-specific Pss knockdown was associated with a decrease in gut size, a change in gut pH, and reduced food intake. These abnormalities affected normal nutrient metabolism in larvae, leading to decreased secretion of Drosophila insulin-like peptides. Consequently, the reduced systemic Akt signaling at the organismal level resulted not only in impaired gut growth but also in abnormal organismal growth and development.

Conclusion: These findings highlight the significant role of the Pss gene in the growth and development of D. melanogaster.

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Pss在中肠中的敲低导致果蝇的生长迟缓，类似于人类LMHD。

背景：磷脂酰丝氨酸合成酶（Phosphatidylserine synthase， PSS）位于线粒体膜上，可合成磷脂酰丝氨酸。在人类中，Pss的突变会导致Lenz-Majewski肥厚性侏儒症，这是一种影响生长发育的疾病。Pss突变对果蝇生长的影响尚不完全清楚。因此，本研究旨在探讨Pss基因敲低对黑腹巨噬菌生长发育的影响。结果：肠细胞（EC）特异性Pss敲低通过Akt信号的减少导致肠道细胞大小的减少。ec特异性Pss敲低与肠道大小减小、肠道pH值变化和食物摄入量减少有关。这些异常影响了幼虫正常的营养代谢，导致果蝇胰岛素样肽分泌减少。因此，机体水平上全身性Akt信号的减少不仅会导致肠道生长受损，还会导致机体生长发育异常。结论：上述结果提示Pss基因在黑腹水蛭生长发育过程中具有重要作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Developmental Dynamics 生物-发育生物学

CiteScore

5.10

自引率

8.00%

发文量

116

审稿时长

3-8 weeks

期刊介绍： Developmental Dynamics, is an official publication of the American Association for Anatomy. This peer reviewed journal provides an international forum for publishing novel discoveries, using any model system, that advances our understanding of development, morphology, form and function, evolution, disease, stem cells, repair and regeneration.