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Identification of Players Controlling Meristem Arrest Downstream of the FRUITFULL-APETALA2 Pathway
Author(s) -
Irene MartínezFernández,
Stéfanie Menezes de Moura,
Márcio AlvesFerreira,
Cristina Ferrándiz,
Vicente Balanzà
Publication year - 2020
Publication title -
plant physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.554
H-Index - 312
eISSN - 1532-2548
pISSN - 0032-0889
DOI - 10.1104/pp.20.00800
Subject(s) - meristem , biology , arabidopsis , microbiology and biotechnology , transcription factor , transcriptome , mitosis , arabidopsis thaliana , gene , genetics , gene expression , mutant
The end of the reproductive phase in monocarpic plants is determined by a coordinated arrest of all active meristems, a process known as global proliferative arrest (GPA). GPA is linked to the correlative control exerted by developing seeds and, possibly, the establishment of strong source-sink relationships. It has been proposed that the meristems that undergo arrest at the end of the reproductive phase behave at the transcriptomic level as dormant meristems, with low mitotic activity and high expression of abscisic acid response genes. Meristem arrest is also controlled genetically. In Arabidopsis ( Arabidopsis thaliana ), the MADS-box transcription factor FRUITFULL induces GPA by directly repressing genes of the APETALA2 ( AP2 ) clade. The AP2 genes maintain shoot apical meristem (SAM) activity in part by keeping WUSCHEL expression active, but the mechanisms downstream of this pathway remain elusive. To identify target genes, we performed a transcriptomic analysis, inducing AP2 activity in meristems close to arrest. Our results suggest that AP2 controls meristem arrest by repressing genes related to axillary bud dormancy in the SAM and negative regulators of cytokinin signaling. In addition, our analysis indicates that genes involved in the response to environmental signals also respond to AP2, suggesting that it could modulate the end of flowering by controlling responses to both endogenous and exogenous signals. Our results support the previous observation that at the end of the reproductive phase the arrested SAM behaves as a dormant meristem, and they strongly support AP2 as a master regulator of this process.

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