The Botrytis cinerea Xylanase BcXyl1 Modulates Plant Immunity

Botrytis cinerea is one of the most notorious pathogenic species that causes serious plant diseases and substantial losses in agriculture throughout the world. We identified BcXyl1 from B. cinerea that exhibited xylanase activity. Expression of the BcXyl1 gene was strongly induced in B. cinerea infe...

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Main Authors: Yuankun Yang, Xiufen Yang, Yijie Dong, Dewen Qiu
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-10-01
Series:Frontiers in Microbiology
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fmicb.2018.02535/full
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spelling doaj-dc0dcd32100a4810ae95c9c1b7bb26ee2020-11-25T01:14:50ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2018-10-01910.3389/fmicb.2018.02535417320The Botrytis cinerea Xylanase BcXyl1 Modulates Plant ImmunityYuankun YangXiufen YangYijie DongDewen QiuBotrytis cinerea is one of the most notorious pathogenic species that causes serious plant diseases and substantial losses in agriculture throughout the world. We identified BcXyl1 from B. cinerea that exhibited xylanase activity. Expression of the BcXyl1 gene was strongly induced in B. cinerea infecting Nicotiana benthamiana and tomato plants, and BcXyl1 deletion strains severely compromised the virulence of B. cinerea. BcXyl1 induced strong cell death in several plants, and cell death activity of BcXyl1 was independent of its xylanase activity. Purified BcXyl1 triggered typically PAMP-triggered immunity (PTI) responses and conferred resistance to B. cinerea and TMV in tobacco and tomato plants. A 26-amino acid peptide of BcXyl1 was sufficient for elicitor function. Furthermore, the BcXyl1 death-inducing signal was mediated by the plant LRR receptor-like kinases (RLKs) BAK1 and SOBIR1. Our data suggested that BcXyl1 contributed to B. cinerea virulence and induced plant defense responses.https://www.frontiersin.org/article/10.3389/fmicb.2018.02535/fullBotrytis cinereaxylanaseBcXyl1plant immunityvirulence
collection DOAJ
language English
format Article
sources DOAJ
author Yuankun Yang
Xiufen Yang
Yijie Dong
Dewen Qiu
spellingShingle Yuankun Yang
Xiufen Yang
Yijie Dong
Dewen Qiu
The Botrytis cinerea Xylanase BcXyl1 Modulates Plant Immunity
Frontiers in Microbiology
Botrytis cinerea
xylanase
BcXyl1
plant immunity
virulence
author_facet Yuankun Yang
Xiufen Yang
Yijie Dong
Dewen Qiu
author_sort Yuankun Yang
title The Botrytis cinerea Xylanase BcXyl1 Modulates Plant Immunity
title_short The Botrytis cinerea Xylanase BcXyl1 Modulates Plant Immunity
title_full The Botrytis cinerea Xylanase BcXyl1 Modulates Plant Immunity
title_fullStr The Botrytis cinerea Xylanase BcXyl1 Modulates Plant Immunity
title_full_unstemmed The Botrytis cinerea Xylanase BcXyl1 Modulates Plant Immunity
title_sort botrytis cinerea xylanase bcxyl1 modulates plant immunity
publisher Frontiers Media S.A.
series Frontiers in Microbiology
issn 1664-302X
publishDate 2018-10-01
description Botrytis cinerea is one of the most notorious pathogenic species that causes serious plant diseases and substantial losses in agriculture throughout the world. We identified BcXyl1 from B. cinerea that exhibited xylanase activity. Expression of the BcXyl1 gene was strongly induced in B. cinerea infecting Nicotiana benthamiana and tomato plants, and BcXyl1 deletion strains severely compromised the virulence of B. cinerea. BcXyl1 induced strong cell death in several plants, and cell death activity of BcXyl1 was independent of its xylanase activity. Purified BcXyl1 triggered typically PAMP-triggered immunity (PTI) responses and conferred resistance to B. cinerea and TMV in tobacco and tomato plants. A 26-amino acid peptide of BcXyl1 was sufficient for elicitor function. Furthermore, the BcXyl1 death-inducing signal was mediated by the plant LRR receptor-like kinases (RLKs) BAK1 and SOBIR1. Our data suggested that BcXyl1 contributed to B. cinerea virulence and induced plant defense responses.
topic Botrytis cinerea
xylanase
BcXyl1
plant immunity
virulence
url https://www.frontiersin.org/article/10.3389/fmicb.2018.02535/full
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