14-3-3Tau regulates Beclin 1 and is required for autophagy.

<h4>Background</h4>Beclin 1 plays an essential role in autophagy; however, the regulation of Beclin 1 expression remains largely unexplored. An earlier ChIP-on-chip study suggested Beclin 1 could be an E2F target. Previously, we also reported that 14-3-3tau regulates E2F1 stability, and...

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Autores principales:	Bing Wang, Shiyun Ling, Weei-Chin Lin
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/67bac095de83498d9aaaed4d3e94fe55
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spelling	oai:doaj.org-article:67bac095de83498d9aaaed4d3e94fe552021-12-02T20:22:02Z14-3-3Tau regulates Beclin 1 and is required for autophagy.1932-620310.1371/journal.pone.0010409https://doaj.org/article/67bac095de83498d9aaaed4d3e94fe552010-04-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20454448/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Beclin 1 plays an essential role in autophagy; however, the regulation of Beclin 1 expression remains largely unexplored. An earlier ChIP-on-chip study suggested Beclin 1 could be an E2F target. Previously, we also reported that 14-3-3tau regulates E2F1 stability, and is required for the expression of several E2F1 target genes. 14-3-3 proteins mediate many cellular signaling processes, but its role in autophagy has not been investigated. We hypothesize that 14-3-3tau could regulate Beclin 1 expression through E2F1 and thus regulate autophagy.<h4>Methods and findings</h4>Using the RNAi technique we demonstrate a novel role for one of 14-3-3 isoforms, 14-3-3tau, in the regulation of Beclin 1 expression and autophagy. Depletion of 14-3-3tau inhibits the expression of Beclin 1 in many different cell lines; whereas, upregulation of 14-3-3tau induces Beclin 1. The regulation is physiologically relevant as an extracellular matrix protein tenascin-C, a known 14-3-3tau inducer, can induce Beclin 1 through 14-3-3tau. Moreover, rapamycin-induced, serum free-induced and amino acid starvation-induced autophagy depends on 14-3-3tau. We also show the expression of Beclin 1 depends on E2F, and E2F can transactivate the Beclin 1 promoter in a promoter reporter assay. Upregulation of Beclin 1 by 14-3-3tau requires E2F1. Depletion of E2F1, like 14-3-3tau, also inhibits autophagy.<h4>Conclusion</h4>Taken together, this study uncovers a role for 14-3-3tau in Beclin 1 and autophagy regulation probably through regulation of E2F1.Bing WangShiyun LingWeei-Chin LinPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 4, p e10409 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Bing Wang Shiyun Ling Weei-Chin Lin 14-3-3Tau regulates Beclin 1 and is required for autophagy.
description	<h4>Background</h4>Beclin 1 plays an essential role in autophagy; however, the regulation of Beclin 1 expression remains largely unexplored. An earlier ChIP-on-chip study suggested Beclin 1 could be an E2F target. Previously, we also reported that 14-3-3tau regulates E2F1 stability, and is required for the expression of several E2F1 target genes. 14-3-3 proteins mediate many cellular signaling processes, but its role in autophagy has not been investigated. We hypothesize that 14-3-3tau could regulate Beclin 1 expression through E2F1 and thus regulate autophagy.<h4>Methods and findings</h4>Using the RNAi technique we demonstrate a novel role for one of 14-3-3 isoforms, 14-3-3tau, in the regulation of Beclin 1 expression and autophagy. Depletion of 14-3-3tau inhibits the expression of Beclin 1 in many different cell lines; whereas, upregulation of 14-3-3tau induces Beclin 1. The regulation is physiologically relevant as an extracellular matrix protein tenascin-C, a known 14-3-3tau inducer, can induce Beclin 1 through 14-3-3tau. Moreover, rapamycin-induced, serum free-induced and amino acid starvation-induced autophagy depends on 14-3-3tau. We also show the expression of Beclin 1 depends on E2F, and E2F can transactivate the Beclin 1 promoter in a promoter reporter assay. Upregulation of Beclin 1 by 14-3-3tau requires E2F1. Depletion of E2F1, like 14-3-3tau, also inhibits autophagy.<h4>Conclusion</h4>Taken together, this study uncovers a role for 14-3-3tau in Beclin 1 and autophagy regulation probably through regulation of E2F1.
format	article
author	Bing Wang Shiyun Ling Weei-Chin Lin
author_facet	Bing Wang Shiyun Ling Weei-Chin Lin
author_sort	Bing Wang
title	14-3-3Tau regulates Beclin 1 and is required for autophagy.
title_short	14-3-3Tau regulates Beclin 1 and is required for autophagy.
title_full	14-3-3Tau regulates Beclin 1 and is required for autophagy.
title_fullStr	14-3-3Tau regulates Beclin 1 and is required for autophagy.
title_full_unstemmed	14-3-3Tau regulates Beclin 1 and is required for autophagy.
title_sort	14-3-3tau regulates beclin 1 and is required for autophagy.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/67bac095de83498d9aaaed4d3e94fe55
work_keys_str_mv	AT bingwang 1433tauregulatesbeclin1andisrequiredforautophagy AT shiyunling 1433tauregulatesbeclin1andisrequiredforautophagy AT weeichinlin 1433tauregulatesbeclin1andisrequiredforautophagy
_version_	1718374111805177856

14-3-3Tau regulates Beclin 1 and is required for autophagy.

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