Plant Bax Inhibitor-1 interacts with ATG6 to regulate autophagy and programmed cell death.

Content Provider	Semantic Scholar
Author	Xu, Guoyong Wang, Shanshan Han, Shaojie Wang, Yan Li, Jinlin Liu, Yule
Copyright Year	2017
Abstract	Autophagy is an evolutionarily conserved catabolic process and is involved in the regulation of programmed cell death during the plant immune response. However, mechanisms regulating autophagy and cell death are incompletely understood. Here, we demonstrate that plant Bax inhibitor-1 (BI-1), a highly conserved cell death regulator, interacts with ATG6, a core autophagy-related protein. Silencing of BI-1 reduced the autophagic activity induced by both N gene-mediated resistance to Tobacco mosaic virus (TMV) and methyl viologen (MV), and enhanced N gene-mediated cell death. In contrast, overexpression of plant BI-1 increased autophagic activity and surprisingly caused autophagy-dependent cell death. These results suggest that plant BI-1 has both prosurvival and prodeath effects in different physiological contexts and both depend on autophagic activity.
Starting Page	1161
Ending Page	1175
Page Count	15
File Format	PDF HTM / HTML
DOI	10.1080/15548627.2017.1320633
PubMed reference number	28537463
Journal	Medline
Volume Number	13
Issue Number	7
Alternate Webpage(s)	http://pdf-s3.xuebalib.com:1262/1gxbkaNbPncu.pdf?down
Alternate Webpage(s)	https://doi.org/10.1080/15548627.2017.1320633
Journal	Autophagy
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article