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PAD4 Mutation Accelerating Programmed Cell Death in Arabidopsis thaliana Tyrosine Degradation Deficient Mutant sscd1

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  • 1College of Bioscience and Biotechnology, Hunan Agricultural University, Changsha 410128, China
    2Yichun University, Yichun 336000, China

Received date: 2021-11-13

  Accepted date: 2022-03-18

  Online published: 2022-03-18

Abstract

Programmed cell death (PCD) is extremely important for plant growth and defense. Fumarylacetoacetate hydrolase (FAH) deficient mutant short-day sensitive cell death 1 (sscd1) displayed PCD under short day condition (8 h light/16 h darkness). Our previous study found PCD in sscd1 was related to jasmonates (JAs) signal transduction but not to salicylic acid (SA). Phytoalexin deficient 4 (PAD4) is involved in mutual antagonism between SA and JAs signaling. In this study, PCD was accompanied by up-regulation of PAD4; while mutation of PAD4 accelerated the sscd1 PCD and induced JAs signaling pathway downstream response genes vegetative storage protein 2thionin2.1 and defensin1.2. In triple mutant sscd1/pad4/coil, JAs signal transduction was blocked, resulting in the disappearance of PCD acceleration. PAD4 mutation induce the expression of Tyr degradation gene homogentisate dioxygenase and maleylacetoacetate isomerase, singlet oxygen specific induced genes bonzai1-associated protein 1 and a putative c2h2 zinc finger transcription factor in sscd1, the induction is dependent on JAs signaling receptor COI1. In conclusion, PAD4 mutation increase JAs signaling, then accelerate tyrosine degradation and singlet oxygen accumulation, thereby promoting PCD in the sscd1 mutant.

Cite this article

Tiantian Zhi, Zhou Zhou, Chengyun Han, Chunmei Ren . PAD4 Mutation Accelerating Programmed Cell Death in Arabidopsis thaliana Tyrosine Degradation Deficient Mutant sscd1[J]. Chinese Bulletin of Botany, 2022 , 57(3) : 288 -298 . DOI: 10.11983/CBB21194

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