Identification of SUMO Proteins and Their Expression Profile During Induction of Somatic Embryogenesis in Medicago truncatula Gaertn.
Somatic embryogenesis (SE) is a key plant regeneration technique involving the reprogramming of somatic cells into embryogenic structures. This developmental transition is regulated by complex genetic and epigenetic mechanisms, including post-translational modifications such as SUMOylation-the covalent attachment of small ubiquitin-like modifier (SUMO) proteins to target proteins, influencing their function, stability, and interactions. While SUMOylation is known to regulate plant development and stress responses, its role in SE has remained unknown. In this study, we investigated the involvement of the SUMOylation pathway in SE induction in <i>Medicago truncatula</i>. Using BLASTp analysis with known SUMO pathway proteins from <i>Arabidopsis thaliana</i> and <i>Glycine max</i>, we identified 10 homologous genes in <i>M. truncatula</i>. Phylogenetic relationships, gene structure, and conserved motif analyses confirmed their evolutionary conservation and characteristic domains. Expression profiling revealed significant upregulation of SUMO pathway genes-including Mt <i>SUMO2</i>, Mt <i>SAE1-2</i>, Mt <i>SCE1a-b</i>, Mt <i>MMS21</i>, and Mt <i>PIAL2</i>-in embryogenic cell lines during early SE induction. Additionally, in silico prediction of SUMOylation sites and SUMO-interacting motifs (SIMs) in 12 key SE regulatory proteins indicated a broad potential for SUMO-mediated regulation. These findings suggest that SUMOylation may contribute to the acquisition of embryogenic competence during somatic cell reprogramming in plants.
Authors
- Paulina Król (ORCID: https://orcid.org/0000-0001-7351-1483)
- Anna Kujawska
Institutions
- University of Szczecin (PL)
Publication Details
- Journal
- International Journal of Molecular Sciences
- Published
- 2025-08-22
- DOI
- https://doi.org/10.3390/ijms26178133
- Primary Topic
- Plant tissue culture and regeneration
- Type
- article
- Field-Weighted Citation Impact
- 0.00