skip to main content
US FlagAn official website of the United States government
dot gov icon
Official websites use .gov
A .gov website belongs to an official government organization in the United States.
https lock icon
Secure .gov websites use HTTPS
A lock ( lock ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.


Search for: All records

Creators/Authors contains: "Yan, Xuemei"

Note: When clicking on a Digital Object Identifier (DOI) number, you will be taken to an external site maintained by the publisher. Some full text articles may not yet be available without a charge during the embargo (administrative interval).
What is a DOI Number?

Some links on this page may take you to non-federal websites. Their policies may differ from this site.

  1. ABSTRACT Necrotrophic pathogens cause serious threats to agricultural crops, and understanding the resistance genes and their genetic networks is key to breeding new plant cultivars with better resistance traits. AlthoughAlternaria alternatacauses black spot in important leafy brassica vegetables, and leads to significant loss of yield and food quality, little is known about plant–A. alternatainteractions. In this study, we used a unique and large collection of single, double and triple mutant lines of defence metabolite regulators inArabidopsisto explore how these transcription factors and their epistatic networks may influenceA. alternatainfections. This identified nine novel regulators and 20 pairs of epistatic interactions that modulateArabidopsisplants' defence responses toA. alternatainfection. We further showed that the glucosinolate 4‐methoxy‐indol‐3‐ylmethyl is the only glucosinolate consistently responsive toA. alternatainfection in Col‐0 ecotype. With the further exploration of the regulators and the genetic networks on modulating the accumulation of glucosinolates underA. alternatainfection, an inverted triangle regulatory model was proposed forArabidopsisplants' defence responses at a metabolic level and a phenotypic level. 
    more » « less
    Free, publicly-accessible full text available February 1, 2026