MERISTEM-DEFECTIVE regulates the balance between stemness and differentiation 
in the root meristem through RNA splicing control

Thompson, H.L.; Shen, W.; Matus, R.; Kakkar, M.; Jones, C.; Dolan, D.; Grellscheid, S.; Yang, X.; Zhang, N.; Mozaffari-Jovin, Sina; Chen, C.; Zhang, X.; Topping, J.F.; Lindsey, K.

doi:10.1242/dev.201476

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MERISTEM-DEFECTIVE regulates the balance between stemness and differentiation in the root meristem through RNA splicing control

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Mozaffari-Jovin, Sina
Emeritus Group of Cellular Biochemistry, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Citation

Thompson, H., Shen, W., Matus, R., Kakkar, M., Jones, C., Dolan, D., et al. (2023). MERISTEM-DEFECTIVE regulates the balance between stemness and differentiation in the root meristem through RNA splicing control. Development, 150(7): dev201476. doi:10.1242/dev.201476.

Cite as: https://hdl.handle.net/21.11116/0000-000D-07B5-F

Abstract

Plants respond to environmental stresses through controlled stem cell maintenance and meristem activity. One level of gene regulation is RNA alternative splicing. However, the mechanistic link between stress, meristem function and RNA splicing is poorly understood. The MERISTEM-DEFECTIVE (MDF) Arabidopsis gene encodes an SR-related family protein, required for meristem function and leaf vascularization, and is the likely orthologue of the human SART1 and yeast Snu66 splicing factors. MDF is required for the correct splicing and expression of key transcripts associated with root meristem function. We identified RSZ33 and ACC1, both known to regulate cell patterning, as splicing targets required for MDF function in the meristem. MDF expression is modulated by osmotic and cold stress, associated with differential splicing and specific isoform accumulation and shuttling between nucleus and cytosol, and acts in part via a splicing target SR34. We propose a model in which MDF controls splicing in the root meristem to promote stemness and to repress stress response, cell differentiation and cell death pathways.