The SNF5-type protein BUSHY regulates seed germination via the gibberellin pathway and is dependent on HUB1 in Arabidopsis

Main conclusion The SNF5-type protein BUSHY plays a role in the regulation of seed germination via the gibberellin pathway dependent on HUB1 in Arabidopsis thaliana. SWITCH/SUCROSE NONFERMENTING (SWI/SNF) complexes play diverse roles in plant development. Some components have roles in embryo development and seed maturation, however, whether the SNF5-type protein BUSHY (BSH), one of the components, plays a role in Arabidopsis seed related traits is presently unclear. In our study, we show that a loss-of-function mutation in BSH causes increased seed germination in Arabidopsis. BSH transcription was induced by the gibberellin (GA) inhibitor paclobutrazol (PAC) in the seed, and BSH regulates the expression of GA pathway genes, such as Gibberellin 3-Oxidase 1 (GA3OX1), Gibberellic Acid-Stimulated Arabidopsis 4 (GASA4), and GASA6 during seed germination. A genetic analysis showed that seed germination was distinctly improved in the bshga3ox1ga3ox2 triple mutant, indicating that BSH acts partially downstream of GA3OX1 and GA3OX2. Moreover, the regulation of seed germination by BSH in response to PAC is dependent on HUB1. These results provide new insights and clues to understand the mechanisms of phytohormones in the regulation of seed germination.

Automated summary

In this study, it was discovered that the SNF5-type protein BUSHY (BSH) plays a role in the regulation of seed germination via the gibberellin pathway dependent on HUB1 in Arabidopsis thaliana. BSH transcription is induced by the gibberellin inhibitor PAC in the seed, and BSH regulates the expression of GA pathway genes during seed germination. Additionally, BSH acts partially downstream of GA3OX1 and GA3OX2, and its regulation of seed germination in response to PAC is dependent on HUB1.