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Short Communication

MYB3R-SCL28-SMR module with a role in cell size control negatively regulates G2 progression in Arabidopsis

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Article: 2153209 | Received 15 May 2022, Accepted 24 Nov 2022, Published online: 28 Dec 2022
 

ABSTRACT

Cell size control is one of the prerequisites for plant growth and development. Recently, a GRAS family transcription factor, SCARECROW-LIKE28 (SCL28), was identified as a critical regulator for both mitotic and postmitotic cell-size control. Here, we show that SCL28 is specifically expressed in proliferating cells and exerts its function to delay G2 progression during mitotic cell cycle in Arabidopsis thaliana. Overexpression of SCL28 provokes a significant enlargement of cells in various organs and tissues, such as leaves, flowers and seeds, to different extents depending on the type of cells. The increased cell size is most likely due to a delayed G2 progression and accelerated onset of endoreplication, an atypical cell cycle repeating DNA replication without cytokinesis or mitosis. Unlike DWARF AND LOW-TILLERING, a rice ortholog of SCL28, SCL28 may not have a role in brassinosteroid (BR) signaling because sensitivity against brassinazole, a BR biosynthesis inhibitor, was not dramatically altered in scl28 mutant and SCL28-overexpressing plants. Collectively, our findings strengthen a recently proposed model of cell size control by SCL28 and suggest the presence of diversified evolutionary mechanisms for the regulation and action of SCL28.

Acknowledgments

The authors thank Asako Segawa, Naoyuki Furuya, Ayako Nakamura, and Ayumi Yamada for technical assistance.

Author contributions

M.I. developed the core idea and designed all the experiments. M.I, H.T., Y.N., A.Y., and K.M. carried out experiments, analyzed data, and wrote the article. K.Y., C.B., and I.T. conducted part of experiments. K.S. and T.N contributed to the design of the experiments.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by The Japan Society for the Promotion of Science KAKENHI (22K06261, 22H04714 to M.I.), Japan Science and Technology Agency (JST grant number JPMJPF2102 to M.I.); and MEXT Leading Initiative for Excellent Young Researchers, and Kanazawa University JIKOCHOKOKU project to H.T.