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PbrATG6 modulates reactive oxygen species metabolism and interacts with PbrTLP15 synergistic enhancement of pear resistance to Botryosphaeria dothidea.

Authors :
Wang Y
Liu Y
Zhang Y
Sun X
Wang F
Xie Z
Qi K
Sun X
Zhang S
Source :
International journal of biological macromolecules [Int J Biol Macromol] 2024 Nov; Vol. 281 (Pt 4), pp. 136663. Date of Electronic Publication: 2024 Oct 17.
Publication Year :
2024

Abstract

Autophagy is vital for plant defense against pathogens, with ATG6 being a key gene in this process. At present, little has been reported on the potential function and molecular mechanisms of ATG6 mediated pathogen resistance in pear. This study investigates the function of the pear homolog of ATG6 (PbrATG6) in resistance to Botryosphaeria dothidea. PbrATG6 is expressed differentially in pear tissues and its expression increases upon infection. Overexpression of PbrATG6 enhances resistance in Arabidopsis and pear calli, while silencing it increases susceptibility. PbrTLP15, a pathogenesis-related protein belonging to the PR5 family, was found that interacts with PbrATG6 by a yeast two-hybrid screening. Yeast two-hybrid, luciferase complementation imaging, bimolecular fluorescence complementation assays and pull-down assays showed that PbrATG6 interacts with PbrTLP15. The transient silencing transgenic assays of PbrATG6 and PbrTLP15 revealed that PbrATG6 could cooperate with PbrTLP15 to regulate pear B. dothidea resistance. In addition, transcriptional analyses of autophagy key genes in pTRV-PbrTLP15 and transmission electron microscopy (TEM) assays also implied that PbrTLP15 does affect autophagy. Hence, PbrATG6 and PbrTLP15 may synergistically enhance pear B. dothidea disease resistance. It provides a new strategy for the study of autophagy in pear disease resistance and enriches the research on pear disease resistance mechanism.<br />Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.<br /> (Copyright © 2024 Elsevier B.V. All rights reserved.)

Details

Language :
English
ISSN :
1879-0003
Volume :
281
Issue :
Pt 4
Database :
MEDLINE
Journal :
International journal of biological macromolecules
Publication Type :
Academic Journal
Accession number :
39423984
Full Text :
https://doi.org/10.1016/j.ijbiomac.2024.136663