In:
PLOS Genetics, Public Library of Science (PLoS), Vol. 17, No. 6 ( 2021-6-28), p. e1009636-
Abstract:
Our previous studies showed that MAN3-mediated mannose plays an important role in plant responses to cadmium (Cd) stress. However, the underlying mechanisms and signaling pathways involved are poorly understood. In this study, we showed that an Arabidopsis MYB4-MAN3-Mannose-MNB1 signaling cascade is involved in the regulation of plant Cd tolerance. Loss-of-function of MNB1 ( m an n ose- b inding-lectin 1) led to decreased Cd accumulation and tolerance, whereas overexpression of MNB1 significantly enhanced Cd accumulation and tolerance. Consistently, expression of the genes involved in the GSH-dependent phytochelatin (PC) synthesis pathway (such as GSH1 , GSH2 , PCS1 , and PCS2 ) was significantly reduced in the mnb1 mutants but markedly increased in the MNB1-OE lines in the absence or presence of Cd stress, which was positively correlated with Cd-activated PC synthesis. Moreover, we found that mannose is able to bind to the GNA-related domain of MNB1, and that mannose binding to the GNA-related domain of MNB1 is required for MAN3-mediated Cd tolerance in Arabidopsis . Further analysis showed that MYB4 directly binds to the promoter of MAN3 to positively regulate the transcript of MAN3 and thus Cd tolerance via the GSH-dependent PC synthesis pathway. Consistent with these findings, overexpression of MAN3 rescued the Cd-sensitive phenotype of the myb4 mutant but not the mnb1 mutant, whereas overexpression of MNB1 rescued the Cd-sensitive phenotype of the myb4 mutant. Taken together, our results provide compelling evidence that a MYB4-MAN3-Mannose-MNB1 signaling cascade regulates cadmium tolerance in Arabidopsis through the GSH-dependent PC synthesis pathway.
Type of Medium:
Online Resource
ISSN:
1553-7404
DOI:
10.1371/journal.pgen.1009636
DOI:
10.1371/journal.pgen.1009636.g001
DOI:
10.1371/journal.pgen.1009636.g002
DOI:
10.1371/journal.pgen.1009636.g003
DOI:
10.1371/journal.pgen.1009636.g004
DOI:
10.1371/journal.pgen.1009636.g005
DOI:
10.1371/journal.pgen.1009636.g006
DOI:
10.1371/journal.pgen.1009636.g007
DOI:
10.1371/journal.pgen.1009636.g008
DOI:
10.1371/journal.pgen.1009636.s001
DOI:
10.1371/journal.pgen.1009636.s002
DOI:
10.1371/journal.pgen.1009636.s003
DOI:
10.1371/journal.pgen.1009636.s004
DOI:
10.1371/journal.pgen.1009636.s005
DOI:
10.1371/journal.pgen.1009636.s006
DOI:
10.1371/journal.pgen.1009636.s007
DOI:
10.1371/journal.pgen.1009636.s008
DOI:
10.1371/journal.pgen.1009636.s009
DOI:
10.1371/journal.pgen.1009636.s010
DOI:
10.1371/journal.pgen.1009636.s011
DOI:
10.1371/journal.pgen.1009636.s012
DOI:
10.1371/journal.pgen.1009636.s013
DOI:
10.1371/journal.pgen.1009636.s014
DOI:
10.1371/journal.pgen.1009636.s015
DOI:
10.1371/journal.pgen.1009636.s016
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2021
detail.hit.zdb_id:
2186725-2
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