Control of protein translation by IP3R-mediated Ca2+ release in Drosophila neuroendocrine cells

The inositol 1,4,5-trisphosphate receptor (IP3R) is one of two Ca2+ channels that gates Ca2+ release from ER-stores. The ligand IP3, generated upon specific G-protein coupled receptor activation, binds to IP3R to release Ca2+ into the cytosol. IP3R also mediates ER-store Ca2+ release into the mitoch...

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Main Authors: Megha, Gaiti Hasan
Format: Article
Language:English
Published: Taylor & Francis Group 2017-10-01
Series:Fly
Subjects:
Online Access:http://dx.doi.org/10.1080/19336934.2017.1384103
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author Megha
Gaiti Hasan
author_facet Megha
Gaiti Hasan
author_sort Megha
collection DOAJ
description The inositol 1,4,5-trisphosphate receptor (IP3R) is one of two Ca2+ channels that gates Ca2+ release from ER-stores. The ligand IP3, generated upon specific G-protein coupled receptor activation, binds to IP3R to release Ca2+ into the cytosol. IP3R also mediates ER-store Ca2+ release into the mitochondria, under basal as well as stimulatory conditions; an activity that influences cellular bioenergetics and thus, cellular growth and proliferation. In Drosophila neuroendocrine cells expressing a hypomorphic mutant of IP3R, we observed reduced protein translation levels. Here, we discuss the possible molecular mechanism for this observation. We hypothesize that the cellular energy sensor, AMPK connects IP3R mediated Ca2+ release into the mitochondria, to protein translation, via the TOR pathway.
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spelling doaj.art-64c5a352ecbc4e308191b603f8fa39d92023-09-21T15:09:08ZengTaylor & Francis GroupFly1933-69341933-69422017-10-0111429029610.1080/19336934.2017.13841031384103Control of protein translation by IP3R-mediated Ca2+ release in Drosophila neuroendocrine cellsMegha0Gaiti Hasan1National Centre for Biological Sciences-TIFR, GKVK CampusNational Centre for Biological Sciences-TIFR, GKVK CampusThe inositol 1,4,5-trisphosphate receptor (IP3R) is one of two Ca2+ channels that gates Ca2+ release from ER-stores. The ligand IP3, generated upon specific G-protein coupled receptor activation, binds to IP3R to release Ca2+ into the cytosol. IP3R also mediates ER-store Ca2+ release into the mitochondria, under basal as well as stimulatory conditions; an activity that influences cellular bioenergetics and thus, cellular growth and proliferation. In Drosophila neuroendocrine cells expressing a hypomorphic mutant of IP3R, we observed reduced protein translation levels. Here, we discuss the possible molecular mechanism for this observation. We hypothesize that the cellular energy sensor, AMPK connects IP3R mediated Ca2+ release into the mitochondria, to protein translation, via the TOR pathway.http://dx.doi.org/10.1080/19336934.2017.1384103ampklarvaestarvationtor
spellingShingle Megha
Gaiti Hasan
Control of protein translation by IP3R-mediated Ca2+ release in Drosophila neuroendocrine cells
Fly
ampk
larvae
starvation
tor
title Control of protein translation by IP3R-mediated Ca2+ release in Drosophila neuroendocrine cells
title_full Control of protein translation by IP3R-mediated Ca2+ release in Drosophila neuroendocrine cells
title_fullStr Control of protein translation by IP3R-mediated Ca2+ release in Drosophila neuroendocrine cells
title_full_unstemmed Control of protein translation by IP3R-mediated Ca2+ release in Drosophila neuroendocrine cells
title_short Control of protein translation by IP3R-mediated Ca2+ release in Drosophila neuroendocrine cells
title_sort control of protein translation by ip3r mediated ca2 release in drosophila neuroendocrine cells
topic ampk
larvae
starvation
tor
url http://dx.doi.org/10.1080/19336934.2017.1384103
work_keys_str_mv AT megha controlofproteintranslationbyip3rmediatedca2releaseindrosophilaneuroendocrinecells
AT gaitihasan controlofproteintranslationbyip3rmediatedca2releaseindrosophilaneuroendocrinecells