TaPP2C-a5 fine-tunes wheat seed dormancy and germination with a Triticeae-specific, alternatively spliced transcript

The sessile plants often experience environmental conditions not ideal for growth, and therefore have evolved strategies to survive and adapt to stress conditions. Abscisic acid (ABA) regulates plant development and abiotic stress response. Clade A type 2C protein phosphatases (PP2Cs), act as co-receptors of ABA, negatively regulate ABA signalling. However, the biological function and detailed molecular mechanism of clade A PP2Cs in ABA signalling pathway remain to be elucidated in wheat.

To analyze the mechanisms of stress response and development mediated by ABA signal precisely regulated by TaPP2C-a5 at the post-transcriptional level in wheat, providing candidate genes for wheat improvement.

Based on our previous results of TaPP2Cs gene family analysis, the function and detailed regulation mechanisms of TaPP2C-a5 gene in seed dormancy and germination as well as drought response mediated by ABA signaling pathway were explored through reverse genetics technology.

We found that class A TaPP2C-a5 underwent alternative splicing (AS) to produce two transcripts encoding TaPP2C-a5.1 and TaPP2C-a5.2, respectively. Both TaPP2C-a5.1 and TaPP2C-a5.2 were highly expressed in mature seeds, and were upregulated by exogenous ABA in seedlings. Overexpression of TaPP2C-a5.1 and TaPP2C-a5.2 coordinately negatively regulated seed dormancy and ABA-mediated seed germination as well as post-germination developmental arrest in wheat. TaPP2C-a5.1 negatively regulated drought stress response, while TaPP2C-a5.2 did not participate in drought stress response. The homologous genes of TaPP2C-a5 underwent the same AS as TaPP2C-a5 in tetraploid wheat, but not in rice.

Our results revealed that TaPP2C-a5 gene underwent AS and was involved in the regulation of seed dormancy and germination, as well as drought stress response mediated by the ABA signaling at the post-transcriptional level. Our work not only provide a potential target gene to improve PHS resistance, but also emphasize alternative splicing as a strategy with evolution contexts to fine-tune ABA signaling and its involvement in certain biological process.