Microtubules and Gαo-signaling modulate the preferential secretion of young insulin secretory granules in islet β cells via independent pathways.

For sustainable function, each pancreatic islet β cell maintains thousands of insulin secretory granules (SGs) at all times. Glucose stimulation induces the secretion of a small portion of these SGs and simultaneously boosts SG biosynthesis to sustain this stock. The failure of these processes, ofte...

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Autores principales:	Ruiying Hu, Xiaodong Zhu, Mingyang Yuan, Kung-Hsien Ho, Irina Kaverina, Guoqiang Gu
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/0229e415c43041759b798e0d2cca4765
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spelling	oai:doaj.org-article:0229e415c43041759b798e0d2cca47652021-12-02T20:04:57ZMicrotubules and Gαo-signaling modulate the preferential secretion of young insulin secretory granules in islet β cells via independent pathways.1932-620310.1371/journal.pone.0241939https://doaj.org/article/0229e415c43041759b798e0d2cca47652021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0241939https://doaj.org/toc/1932-6203For sustainable function, each pancreatic islet β cell maintains thousands of insulin secretory granules (SGs) at all times. Glucose stimulation induces the secretion of a small portion of these SGs and simultaneously boosts SG biosynthesis to sustain this stock. The failure of these processes, often induced by sustained high-insulin output, results in type 2 diabetes. Intriguingly, young insulin SGs are more likely secreted during glucose-stimulated insulin secretion (GSIS) for unknown reasons, while older SGs tend to lose releasability and be degraded. Here, we examine the roles of microtubule (MT) and Gαo-signaling in regulating the preferential secretion of young versus old SGs. We show that both MT-destabilization and Gαo inactivation results in more SGs localization near plasma membrane (PM) despite higher levels of GSIS and reduced SG biosynthesis. Intriguingly, MT-destabilization or Gαo-inactivation results in higher secretion probabilities of older SGs, while combining both having additive effects on boosting GSIS. Lastly, Gαo inactivation does not detectably destabilize the β-cell MT network. These findings suggest that Gαo and MT can modulate the preferential release of younger insulin SGs via largely parallel pathways.Ruiying HuXiaodong ZhuMingyang YuanKung-Hsien HoIrina KaverinaGuoqiang GuPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 7, p e0241939 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ruiying Hu Xiaodong Zhu Mingyang Yuan Kung-Hsien Ho Irina Kaverina Guoqiang Gu Microtubules and Gαo-signaling modulate the preferential secretion of young insulin secretory granules in islet β cells via independent pathways.
description	For sustainable function, each pancreatic islet β cell maintains thousands of insulin secretory granules (SGs) at all times. Glucose stimulation induces the secretion of a small portion of these SGs and simultaneously boosts SG biosynthesis to sustain this stock. The failure of these processes, often induced by sustained high-insulin output, results in type 2 diabetes. Intriguingly, young insulin SGs are more likely secreted during glucose-stimulated insulin secretion (GSIS) for unknown reasons, while older SGs tend to lose releasability and be degraded. Here, we examine the roles of microtubule (MT) and Gαo-signaling in regulating the preferential secretion of young versus old SGs. We show that both MT-destabilization and Gαo inactivation results in more SGs localization near plasma membrane (PM) despite higher levels of GSIS and reduced SG biosynthesis. Intriguingly, MT-destabilization or Gαo-inactivation results in higher secretion probabilities of older SGs, while combining both having additive effects on boosting GSIS. Lastly, Gαo inactivation does not detectably destabilize the β-cell MT network. These findings suggest that Gαo and MT can modulate the preferential release of younger insulin SGs via largely parallel pathways.
format	article
author	Ruiying Hu Xiaodong Zhu Mingyang Yuan Kung-Hsien Ho Irina Kaverina Guoqiang Gu
author_facet	Ruiying Hu Xiaodong Zhu Mingyang Yuan Kung-Hsien Ho Irina Kaverina Guoqiang Gu
author_sort	Ruiying Hu
title	Microtubules and Gαo-signaling modulate the preferential secretion of young insulin secretory granules in islet β cells via independent pathways.
title_short	Microtubules and Gαo-signaling modulate the preferential secretion of young insulin secretory granules in islet β cells via independent pathways.
title_full	Microtubules and Gαo-signaling modulate the preferential secretion of young insulin secretory granules in islet β cells via independent pathways.
title_fullStr	Microtubules and Gαo-signaling modulate the preferential secretion of young insulin secretory granules in islet β cells via independent pathways.
title_full_unstemmed	Microtubules and Gαo-signaling modulate the preferential secretion of young insulin secretory granules in islet β cells via independent pathways.
title_sort	microtubules and gαo-signaling modulate the preferential secretion of young insulin secretory granules in islet β cells via independent pathways.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/0229e415c43041759b798e0d2cca4765
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Microtubules and Gαo-signaling modulate the preferential secretion of young insulin secretory granules in islet β cells via independent pathways.

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