Abstract

Spliceosomes are large protein-RNA complexes regulating pre-mRNA processing in eukaryotes. SF3b4 encodes a core subunit of the U2-type spliceosome, loss- or gain-of-function of which often associates with abnormal cell growth, leading to tumorigenesis. Homologs of SF3b4 in other phyla are also essential. In this review, we summarize recent findings on the function of SF3b4. Importantly, we highlight the versatile roles of SF3b4, not only as a component for pre-mRNA splicing, but also as a regulator for transcription, translation, and cell signaling. Recent studies of SF3b4 homologs in different species across evolution will facilitate a better understanding of human diseases caused by the malfunction of SF3b4, such as Nager syndrome (NS) and cancer, in the future.

Highlights

  • In eukaryotic cells, pre-mRNA splicing is an important step for gene expression with precise removal of introns from pre-mRNA to give rise to mature mRNA

  • SF3b4 interacts with another spliceosome component SF3b145, and forms a protein complex that is thought to mediate the tethering of U2 snRNP to the branch site of pre-mRNAs (Champion-Arnaud and Reed, 1994; Gozani et al, 1996)

  • Recent studies of SF3b4 in different species across evolution (Watanabe et al, 2007; Ueno et al, 2019; Xiong et al, 2019) have revealed the multiple roles that SF3b4 plays in transcription, in translation, in cell signaling in addition to the traditional pre-mRNA splicing

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Summary

Introduction

Pre-mRNA splicing is an important step for gene expression with precise removal of introns from pre-mRNA to give rise to mature mRNA. SF3b4 interacts with another spliceosome component SF3b145, and forms a protein complex that is thought to mediate the tethering of U2 snRNP to the branch site of pre-mRNAs (Champion-Arnaud and Reed, 1994; Gozani et al, 1996). On the other hand, overexpressing SF3b4 can promote tumorigenesis in hepatocellular carcinoma (HCC) (Liu et al, 2018; Shen et al, 2018), suggesting an essential role of SF3b4 in cell growth.

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