An unexpected role for tomato threonine deaminase 2 in host defense against bacterial infection
An unexpected role for tomato threonine deaminase 2 in host defense against bacterial infection
复制标题
DOI:
10.1093/plphys/kiac584
复制
发表时间:
2022-12-19
期刊:
影响因子:
7.4
通讯作者:
Devarenne,Timothy P.
中科院分区:
文献类型:
--
作者:
Yeo,In-Cheol;de Azevedo Manhaes,Ana Marcia Escocard;Devarenne,Timothy P.
The hormones salicylic acid (SA) and jasmonic acid (JA) often act antagonistically in controlling plant defense pathways in response to hemibiotrophs/biotrophs (hemi/biotroph) and herbivores/necrotrophs, respectively. Threonine deaminase (TD) converts threonine to α-ketobutyrate and ammonia as the committed step in isoleucine (Ile) biosynthesis and contributes to JA responses by producing the Ile needed to make the bioactive JA–Ile conjugate. Tomato (Solanum lycopersicum) plants have twoTDgenes:TD1andTD2. A defensive role for TD2 against herbivores has been characterized in relation to JA–Ile production. However, it remains unknown whether TD2 is also involved in host defense against bacterial hemi/biotrophic and necrotrophic pathogens. Here, we show that in response to the bacterial pathogen-associated molecular pattern (PAMP) flagellin flg22 peptide, an activator of SA-based defense responses, TD2 activity is compromised, possibly through carboxy-terminal cleavage.TD2knockdown (KD) plants showed increased resistance to the hemibiotrophic bacterial pathogenPseudomonas syringaebut were more susceptible to the necrotrophic fungal pathogenBotrytis cinerea, suggesting TD2 plays opposite roles in response to hemibiotrophic and necrotrophic pathogens. ThisTD2KD plant differential response to different pathogens is consistent with SA- and JA-regulated defense gene expression. flg22-treatedTD2KD plants showed high expression levels of SA-responsive genes, whereasTD2KD plants treated with the fungal PAMP chitin showed low expression levels of JA-responsive genes. This study indicates TD2 acts negatively in defense against hemibiotrophs and positively against necrotrophs and provides insight into a new TD2 function in the elaborate crosstalk between SA and JA signaling induced by pathogen infection.