Hypermorphic SERK1 Mutations Function via a SOBIR1 Pathway to Activate Floral Abscission Signaling.

Area of Science:

• Plant Biology
• Molecular Plant Science
• Genetics and Genomics

Background:

• Floral organ abscission in Arabidopsis thaliana is controlled by receptor-like kinases HAESA (HAE) and HAESA-LIKE2 (HSL2).
• HAE/HSL2 signaling is activated by INFLORESCENCE DEFICIENT IN ABSICSSION ligand, requiring SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE (SERK) coreceptors to trigger abscission gene expression.
• Mutations in HAE and HSL2 (hae hsl2) result in persistent floral organs due to failed abscission signaling.

Purpose of the Study:

• To identify genetic suppressors of the abscission defect in Arabidopsis hae hsl2 mutants.
• To elucidate the molecular mechanisms by which SERK1 gain-of-function mutations restore floral organ abscission.
• To investigate the role of SERK1 kinase activity and its interaction with other signaling components like SOBIR1 and BIR1.

Main Methods:

• Isolation and characterization of an allelic series of suppressor mutations in SERK1 within the hae hsl2 background.
• Genetic analysis to confirm the suppressor phenotype and epistasis relationships.
• Transcriptomic profiling to assess gene expression changes related to abscission signaling.
• Biochemical assays to evaluate the role of SERK1 kinase activity and interactions with SOBIR1 and BAK1-INTERACTING RECEPTOR-LIKE KINASE1 (BIR1).

Main Results:

• Identification of novel gain-of-function alleles in SERK1 that suppress the hae hsl2 abscission defect.
• These SERK1 mutations activate abscission signaling independently of HAE/HSL2 and do not require SERK1 kinase activity.
• Signaling activation is dependent on SUPPRESSOR OF BIR1 (SOBIR1) and can be mimicked by loss-of-function mutations in BAK1-INTERACTING RECEPTOR-LIKE KINASE1 (BIR1).

Conclusions:

• Gain-of-function SERK1 mutations provide a new mechanism to activate abscission signaling independently of canonical HAE/HSL2 perception.
• The suppression mechanism highlights a crucial role for SERK1-SOBIR1 signaling in floral abscission.
• BAK1-INTERACTING RECEPTOR-LIKE KINASE1 (BIR1) acts as a negative regulator of SERK-SOBIR1 signaling, and SERK1 mutations likely disrupt this inhibition.