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The TERMINAL FLOWER1-NODULE ROOTs-FRUITFULLc module orchestrates compound inflorescence development in Medicago truncatula
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Y
J
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DOI：10.1093/plcell/koag099.png)
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Abstract
En 中文
Arresting the growth of inflorescence meristems causes a coordinated cessation of flowering that optimizes resource allocation for seed filling. Orthologs of Arabidopsis thaliana TERMINAL FLOWER1 (TFL1) regulate inflorescence meristem activity in various species, maintaining the proliferative phase and meristem indeterminacy. However, the mechanism regulating TFL1-mediated inflorescence meristem activity remains largely unknown, especially in species with compound inflorescences. Compound inflorescences are characterized by a secondary inflorescence (I2) produced by the primary inflorescence (I1) meristem, but the specific genes determining the number of I2 per node remain unclear. Here, we revealed that the arrest of the proliferative phase in Medicago truncatula is ensured through NODULE ROOTs (MtNOOTs)-mediated degradation of MtTFL1. Our results demonstrated that MtNOOTs repress the expression of FRUITFULLc (MtFULc), an I2 identity gene, thereby restricting the outgrowth of I2. We also showed that MtNOOTs-mediated protein turnover of MtTFL1 may contribute to this repression. MtTFL1 maintains I1 meristem activity and MtFULc controls I2 meristem outgrowth, whereas MtNOOTs limit these activities to control I1 meristem activity and restrict the outgrowth of the I2 meristem in the compound inflorescence of M. truncatula. MtNOOTs regulate compound inflorescence architecture in the legume model species Medicago truncatula by modulating MtTFL1 protein level and MtFULc transcription.
Keywords:
GROWTH HABIT
ARABIDOPSIS
PROTEIN
LEAF
BLADE-ON-PETIOLE1
ARCHITECTURE
DETERMINATE
SENESCENCE
INITIATION
INDUCTION
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