4.7 Article

Over-expression of SlWRKY46 in tomato plants increases susceptibility to Botrytis cinerea by modulating ROS homeostasis and SA and JA signaling pathways

期刊

PLANT PHYSIOLOGY AND BIOCHEMISTRY
卷 166, 期 -, 页码 1-9

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ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.plaphy.2021.05.021

关键词

Over-expression; B. cinerea; Tomato plants; SlWRKY46

资金

  1. National Natural Science Foundation of China [32072283]
  2. Natural Science Foundation of Beijing [6202018]

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SlWRKY46 plays a negative regulatory role in B. cinerea infection, potentially by inhibiting the activities of antioxidants and disease resistance enzymes, regulating SA and JA signaling pathways, and modulating ROS homeostasis.
WRKY, as one of the largest families of transcription factors (TFs), binds to cis-acting elements of downstream genes to regulate biotic and abiotic stress. However, the role of SlWRKY46 in fungal disease response induced by Botrytis cinerea (B.cinerea) and potential mechanism remains obscure. To ascertain the role of SlWRKY46 in response to B.cinerea, we constructed SlWRKY46-overexpression plants, which were then inoculated with B. cinerea. SlWRKY46-overexpression plants were more susceptible to B.cinerea and accompanied by the inhibited activities of phenylalanine ammonialyase (PAL), polyphenol oxidase (PPO), chitinase (CHI), and beta-1,3-glucanase (GLU). Additionally, SlWRKY46-overexpression plants showed the decreased activities of ascorbate peroxidase (APX), superoxide dismutase (SOD) and the content of H2O2, and the increased content of O-2(center dot-). Moreover, overexpression of SlWRKY46 suppressed the salicylic acid (SA) and jasmonic acid (JA) marker genes, pathogenesis related protein (PR1), and proteinase inhibitors (PI I and PI II) and consequently aggravated the disease symptoms. Therefore, we speculated that SlWRKY46 played negative regulatory roles in B. cinerea infection probably by inhibiting the activities of antioxidants and disease resistance enzymes, regulating SA and JA signaling pathways and modulating reactive oxygen (ROS) homeostasis.

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