Leaf senescence can be induced by stress or aging, sometimes in a synergistic manner. It is generally acknowledged that the ability to withstand senescence-inducing conditions can provide plants with stress resilience. Although the signaling and transcriptional networks responsible for a delayed senescence phenotype, often referred to as a functional stay-green trait, have been actively investigated, very little is known about the subsequent metabolic adjustments conferring this aptitude to survival. First, using the individually darkened leaf (IDL) experimental setup, we compared IDLs of wild-type (WT) Arabidopsis (Arabidopsis thaliana) to several stay-green contexts, that is IDLs of two functional stay-green mutant lines, oresara1-2 (ore1-2) and an allele of phytochrome-interacting factor 5 (pif5), as well as to leaves from a WT plant entirely darkened (DP). We provide compelling evidence that arginine and ornithine, which accumulate in all stay-green contexts-likely due to the lack of induction of amino acids (AAs) transport-can delay the progression of senescence by fueling the Krebs cycle or the production of polyamines (PAs). Secondly, we show that the conversion of putrescine to spermidine (SPD) is controlled in an age-dependent manner. Thirdly, we demonstrate that SPD represses senescence via interference with ethylene signaling by stabilizing the ETHYLENE BINDING FACTOR1 and 2 (EBF1/2) complex. Taken together, our results identify arginine and ornithine as central metabolites influencing the stress- and age-dependent progression of leaf senescence. We propose that the regulatory loop between the pace of the AA export and the progression of leaf senescence provides the plant with a mechanism to fine-tune the induction of cell death in leaves, which, if triggered unnecessarily, can impede nutrient remobilization and thus plant growth and survival.

• MeSH
• Arabidopsis * metabolismus   MeSH
• arginin metabolismus   MeSH
• ethyleny metabolismus   MeSH
• listy rostlin metabolismus   MeSH
• ornithin genetika   metabolismus   MeSH
• proteiny huseníčku * metabolismus   MeSH
• regulace genové exprese u rostlin MeSH
• senescence rostlin MeSH
• transkripční faktory metabolismus   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• arginin MeSH
• ethyleny MeSH
• ornithin MeSH
• proteiny huseníčku * MeSH
• transkripční faktory MeSH

Alterations of hydrogen peroxide (H2O2) levels have a profound impact on numerous signaling cascades orchestrating plant growth, development, and stress signaling, including programmed cell death. To expand the repertoire of known molecular mechanisms implicated in H2O2 signaling, we performed a forward chemical screen to identify small molecules that could alleviate the photorespiratory-induced cell death phenotype of Arabidopsisthaliana mutants lacking H2O2-scavenging capacity by peroxisomal catalase2. Here, we report the characterization of pakerine, an m-sulfamoyl benzamide from the sulfonamide family. Pakerine alleviates the cell death phenotype of cat2 mutants exposed to photorespiration-promoting conditions and delays dark-induced senescence in wild-type Arabidopsis leaves. By using a combination of transcriptomics, metabolomics, and affinity purification, we identified abnormal inflorescence meristem 1 (AIM1) as a putative protein target of pakerine. AIM1 is a 3-hydroxyacyl-CoA dehydrogenase involved in fatty acid β-oxidation that contributes to jasmonic acid (JA) and salicylic acid (SA) biosynthesis. Whereas intact JA biosynthesis was not required for pakerine bioactivity, our results point toward a role for β-oxidation-dependent SA production in the execution of H2O2-mediated cell death.

• Klíčová slova
• H2O2 signaling, abnormal inflorescence meristem 1, catalase2-deficient Arabidopsis, chemical genetics, photorespiration,
• MeSH
• Arabidopsis cytologie   účinky léků   genetika   metabolismus   MeSH
• buněčná smrt účinky léků   MeSH
• buněčné dýchání účinky léků   genetika   MeSH
• cyklopentany metabolismus   MeSH
• fotosyntéza účinky léků   genetika   MeSH
• fyziologický stres MeSH
• hydroponie metody   MeSH
• kyselina salicylová metabolismus   MeSH
• listy rostlin cytologie   účinky léků   metabolismus   MeSH
• meristém cytologie   účinky léků   metabolismus   MeSH
• multienzymové komplexy genetika   metabolismus   MeSH
• oxylipiny metabolismus   MeSH
• peroxid vodíku antagonisté a inhibitory   farmakologie   MeSH
• proteiny huseníčku genetika   metabolismus   MeSH
• regulace genové exprese u rostlin * MeSH
• rostlinné buňky účinky léků   metabolismus   MeSH
• semena rostlinná účinky léků   MeSH
• signální transdukce MeSH
• stanovení celkové genové exprese MeSH
• sulfonamidy chemická syntéza   farmakologie   MeSH
• transkriptom MeSH
• výpočetní biologie metody   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• AIM1 protein, Arabidopsis MeSH Prohlížeč
• CAT2 protein, Arabidopsis MeSH Prohlížeč
• cyklopentany MeSH
• jasmonic acid MeSH Prohlížeč
• kyselina salicylová MeSH
• multienzymové komplexy MeSH
• oxylipiny MeSH
• peroxid vodíku MeSH
• proteiny huseníčku MeSH
• sulfonamidy MeSH