Abstract

The Arabidopsis gynoecium is a complex structure composed of different tissues. Development is regulated by hormone interactions, especially auxin and cytokinin, as well as the spatiotemporal action of transcription factors and chromatin dynamics, including epigenetic modifications of core histones. SPT is bHLH transcription factor involved in gynoecium development, specifically affecting both auxin and cytokinin responses. GCN5 is a histone acetyltransferase with pleiotropic biological roles including auxin and cytokinin responses in the gynoecium. CLV1 is a receptor kinase, part of the CLAVATA signaling pathway which suppresses the expression of WUS in apical and floral meristems. Previous work has shown that clv1gcn5 double mutants exhibit a plethora of phenotypes including fasciated meristems and abnormal flowers with increased number of stamen and elongated gynoecia with enlarged apical regions and reduced ovaries. In the double mutants, the stem-cell-promoting transcription factor WUS is ectopically overexpressed in the gynoecia. To elucidate genetic interactions between SPT, CLV1 and GCN5 we created all genetic combination between spt, clv1 and gcn5 mutants. We show here that spt mutations largely suppress the phenotypes of clv1gcn5 gynoecia. The enlarged stigma and style and ovary formation are restored in sptclv1gcn5 plants compared to clv1gcn5 plants. The spt mutation also reverses the WUS ectopic overexpression in clv1gcn5 gynoecia. Interestingly spt gynoecia have also reduced WUS expression compared to wild type. These results suggest that SPT mediates the CLV1-GCN5 synergistic interaction during gynoecium development, potentially acting as a positive regulator of WUS expression in the gynoecium.

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.