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Plant Physiol. 2019 Apr 11. pii: pp.01328.2018. doi: 10.1104/pp.18.01328. [Epub ahead of print]

Hypermorphic SERK1 mutations function via a SOBIR1 pathway to activate floral abscission signaling.

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Duke University and Howard Hughes Medical Institute CITY: Durham STATE: North Carolina United States Of America [US].
Washington University in St. Louis CITY: St. Louis STATE: Missouri United States Of America [US].
Washington University in St. Louis CITY: St. Louis United States Of America [US].
University of Missouri CITY: Columbia STATE: Missouri POSTAL_CODE: 65211 United States Of America [US]


In Arabidopsis (Arabidopsis thaliana), the abscission of floral organs is regulated by two related receptor-like protein kinases, HAESA (HAE) and HAESA-like 2 (HSL2). In complex with members of the SERK family of co-receptor protein kinases, HAE and HSL2 are activated when bound by INFLORESCENCE DEFICIENT IN ABSICSSION (IDA), a proteolytically processed peptide ligand, activating the expression of genes encoding secreted cell wall remodeling and hydrolase enzymes. hae hsl2 mutants fail to induce expression of these genes and retain floral organs indefinitely. Here, we report identification of an allelic series of hae hsl2 suppressor mutations in the SERK1 co-receptor protein kinase gene. Genetic and transcriptomic evidence indicates these alleles represent a novel class of gain-of-function mutations that activate signaling independently of HAE/HSL2. We show that, surprisingly, the suppression effect does not rely on the protein kinase activity of SERK1, and that activation of signaling relies on the receptor-like kinase gene SUPPRESSOR OF BIR1 (SOBIR1). The effect of these mutations can be mimicked by loss-of-function of BAK1-INTERACTING RECEPTOR-LIKE KINASE 1 (BIR1), a known negative regulator of SERK-SOBIR1 signaling. These results suggest that BIR1 negatively regulates SERK-SOBIR1 signaling during abscission, and that the identified SERK1 mutations likely interfere with this negative regulation.


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