Major Latex Protein MdMLP423 Negatively Regulates Defense against Fungal Infections in Apple
Major latex proteins (MLPs) play critical roles in plants defense and stress responses. However, the roles of from apple ( ) have not been clearly identified. In this study, we focused on the biological role of , which had been previously characterized as a potential pathogenesis-related gene. Phylo...
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Published in | International journal of molecular sciences Vol. 21; no. 5; p. 1879 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
MDPI AG
10.03.2020
MDPI |
Subjects | |
Online Access | Get full text |
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Summary: | Major latex proteins (MLPs) play critical roles in plants defense and stress responses. However, the roles of
from apple (
) have not been clearly identified. In this study, we focused on the biological role of
, which had been previously characterized as a potential pathogenesis-related gene. Phylogenetic analysis and conserved domain analysis indicated that
is a protein with a 'Gly-rich loop' (GXGGXG) domain belonging to the Bet v_1 subfamily. Gene expression profiles showed that
is mainly expressed in flowers. In addition, the expression of
was significantly inhibited by
f. sp.
(BB) and
apple pathotype (AAAP) infections. Apple calli overexpressing
had lower expression of resistance-related genes, and were more sensitive to infection with BB and AAAP compared with non-transgenic calli. RNA-seq analysis of
-overexpressing calli and non-transgenic calli indicated that
regulated the expression of a number of differentially expressed genes (DEGs) and transcription factors, including genes involved in phytohormone signaling pathways, cell wall reinforcement, and genes encoding the defense-related proteins, AP2-EREBP, WRKY, MYB, NAC, Zinc finger protein, and ABI3. Taken together, our results demonstrate that
negatively regulates apple resistance to BB and AAAP infections by inhibiting the expression of defense- and stress-related genes and transcription factors. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. |
ISSN: | 1422-0067 1661-6596 1422-0067 |
DOI: | 10.3390/ijms21051879 |