Spliceosomal protein U2Bâ³ delays leaf senescence by enhancing splicing variant JAZ9ß expression to attenuate jasmonate signaling in Arabidopsis.
New Phytol
; 240(3): 1116-1133, 2023 Nov.
Article
em En
| MEDLINE
| ID: mdl-37608617
ABSTRACT
The regulatory framework of leaf senescence is gradually becoming clearer; however, the fine regulation of this process remains largely unknown. Here, genetic analysis revealed that U2 small nuclear ribonucleoprotein B (U2Bâ³), a component of the spliceosome, is a negative regulator of leaf senescence. Mutation of U2Bâ³ led to precocious leaf senescence, whereas overexpression of U2Bâ³ extended leaf longevity. Transcriptome analysis revealed that the jasmonic acid (JA) signaling pathway was activated in the u2bâ³ mutant. U2Bâ³ enhances the generation of splicing variant JASMONATE ZIM-DOMAIN 9ß (JAZ9ß) with an intron retention in the Jas motif, which compromises its interaction with CORONATINE INSENSITIVE1 and thus enhances the stability of JAZ9ß protein. Moreover, JAZ9ß could interact with MYC2 and obstruct its activity, thereby attenuating JA signaling. Correspondingly, overexpression of JAZ9ß rescued the early senescence phenotype of the u2bâ³ mutant. Furthermore, JA treatment promoted expression of U2Bâ³ that was found to be a direct target of MYC2. Overexpression of MYC2 in the u2bâ³ mutant resulted in a more pronounced premature senescence than that in wild-type plants. Collectively, our findings reveal that the spliceosomal protein U2Bâ³ fine-tunes leaf senescence by enhancing the expression of JAZ9ß and thereby attenuating JA signaling.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
New Phytol
Ano de publicação:
2023
Tipo de documento:
Article