Abstract

Histone acetylation is known to affect the speed of seed germination, but the molecular regulatory basis of this remains ambiguous. Here we report that loss of function of two histone deacetylase-binding factors, SWI-INDEPENDENT3 (SIN3)-LIKE1 (SNL1) and SNL2, results in accelerated radicle protrusion and growth during seed germination. AUXIN RESISTANT 1 (AUX1) is identified as a key factor in this process, enhancing germination speed downstream of SNL1 and SNL2. AUX1 expression and histone H3 acetylation at lysines 9 and 18 is regulated by SNL1 and SNL2. The D-type cyclins encoding genes CYCD1;1 and CYCD4;1 display increased expression in AUX1 over-expression lines and the snl1snl2 double mutant. Accordingly, knockout of CYCD4;1 reduces seed germination speed of AUX1 over-expression lines and snl1snl2 suggesting the importance of cell cycling for radicle protrusion during seed germination. Together, our work identifies AUX1 as a link between histone acetylation mediated by SNL1 and SNL2, and radicle growth promoted by CYCD1;1 and CYCD4;1 during seed germination.

Highlights

  • Histone acetylation is known to affect the speed of seed germination, but the molecular regulatory basis of this remains ambiguous

  • Transcriptomic studies have shown that RNAs encoding the auxin transporters AUXIN RESISTANT 1 (AUX1), PIN-FORMED 2 (PIN2) and PIN7 were highly upregulated in response to gibberellic acid (GA) treatment of ga[1] mutant seeds[20]

  • We have previously shown that SNL1 and SNL2 are components of the SNL-HDA19 histone deacetylation complex and that they regulate seed dormancy by deacetylating histone H3K9/18 sites of abscisic acid (ABA) and ethylene signalling-related genes[32]

Read more

Summary

Introduction

Histone acetylation is known to affect the speed of seed germination, but the molecular regulatory basis of this remains ambiguous. AUXIN RESPONSE FACTORS (ARF) 10/16 act as positive regulators of the ABA signal pathway by regulating expression of ABI3, and the arf10arf[16] double mutant showed insensitivity for seed germination to ABA18. Transgenic seeds expressing a miR160-resistant form of ARF10 (mARF10) were hypersensitive to germination inhibition by exogenous ABA, whereas ectopic expression of miR160 resulted in a reduced sensitivity to ABA15. AUX1 is required for ABA inhibition of seed germination, loss-of-function mutants of AUX1 showed increased ABA resistance[22] These results indicate that distinct auxin signalling pathways are involved in seed germination by affecting ABA and/or GA signal pathways. These functions of auxin are commonly achieved through the auxin transport carriers in the root tip among which AUX1 has an important role[23]

Methods
Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.