Regulation of PI4P levels by PI4KIIIα during G-protein coupled PLC signaling in Drosophila photoreceptors

Author:

Balakrishnan Sruthi S.1,Basu Urbashi1,Shinde Dhananjay1,Thakur Rajan1,Jaiswal Manish2,Raghu Padinjat1

Affiliation:

1. National Centre for Biological Sciences-TIFR, GKVK Campus, Bellary Road, Bangalore 560065, India

2. TIFR Center for Interdisciplinary Science, Hyderabad, 500107, India

Abstract

The activation of phospholipase C (PLC) is a conserved mechanism of receptor activated cell signaling at the plasma membrane. PLC hydrolyzes the minor membrane lipid phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2] and continued signaling requires the resynthesis and availability of PI(4,5)P2 at the plasma membrane. PI(4,5)P2 is synthesized by the phosphorylation of phosphatidylinositol-4-phosphate (PI4P). Thus, a continuous supply of PI4P is essential to support ongoing PLC signaling. While the enzyme PI4KA has been identified to perform this function in cultured mammalian cells, its function in the context of an in vivo physiological model has not been established. In this study, we show that in Drosophila photoreceptors, PI4KIIIα activity is required to support signaling during G-protein coupled PLC activation. Depletion of PI4KIIIα results in impaired electrical responses to light and reduced plasma membrane levels of PI4P and PI(4,5)P2. Depletion of conserved proteins Efr3 and TTC7 that assemble PI4KIIIα at the plasma membrane also results in an impaired light response and reduced plasma membrane PI4P and PI(4,5)P2 levels. Thus PI4KIIIα activity at the plasma membrane generates PI4P and supports PI(4,5)P2 levels during receptor activated PLC signaling.

Funder

DBT India Alliance

Publisher

The Company of Biologists

Subject

Cell Biology

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3