SON controls cell-cycle progression by coordinated regulation of RNA splicing.

Eun-Young Ahn, Russell C DeKelver, Miao-Chia Lo, Tuyet Ann Nguyen, Shinobu Matsuura, Anita Boyapati, Shatakshi Pandit, Xiang-Dong Fu, Dong-Er Zhang

Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093, USA.

Molecular cell 2011 Apr 22

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It has been suspected that cell-cycle progression might be functionally coupled with RNA processing. However, little is known about the role of the precise splicing control in cell-cycle progression. Here, we report that SON, a large Ser/Arg (SR)-related protein, is a splicing cofactor contributing to efficient splicing of cell-cycle regulators. Downregulation of SON leads to severe impairment of spindle pole separation, microtubule dynamics, and genome integrity. These molecular defects result from inadequate RNA splicing of a specific set of cell-cycle-related genes that possess weak splice sites. Furthermore, we show that SON facilitates the interaction of SR proteins with RNA polymerase II and other key spliceosome components, suggesting its function in efficient cotranscriptional RNA processing. These results reveal a mechanism for controlling cell-cycle progression through SON-dependent constitutive splicing at suboptimal splice sites, with strong implications for its role in cancer and other human diseases. Copyright © 2011 Elsevier Inc. All rights reserved.

Citation

Eun-Young Ahn, Russell C DeKelver, Miao-Chia Lo, Tuyet Ann Nguyen, Shinobu Matsuura, Anita Boyapati, Shatakshi Pandit, Xiang-Dong Fu, Dong-Er Zhang. SON controls cell-cycle progression by coordinated regulation of RNA splicing. Molecular cell. 2011 Apr 22;42(2):185-98