This research demonstrates how splicing factor 30 influences floral transition in Arabidopsis, revealing alternative splicing implications.
Splicing factor 30 (SPF30) is a pivotal spliceosomal protein in human pre-mRNA splicing; however, its function in plants remains unclear. Previously, we identified the SPF30 genes throughout the plant kingdom and found that they have a conserved second intron that undergoes frequent alternative splicing (AS). In this study, we characterized SPF30 and its various alternative isoforms in Arabidopsis (Arabidopsis thaliana). Loss-of-function mutation in SPF30 caused early flowering and impaired expression and splicing of the floral repressor FLOWERING LOCUS C (FLC). Subsequent genetic and molecular analyses further suggested that SFP30 may regulate floral transition mostly through FLC. The primary transcript, SPF30.1, encodes a functional splicing factor associated with spliceosomal core proteins, while isoforms retaining a partial fragment of the second intron are subjected to nonsense-mediated mRNA decay (NMD). Moreover, a long, NMD-immune isoform with the entire second intron retained can be further processed to either SPF30.1 or NMD-sensitive isoforms, potentially enabling the fine-tuning of SPF30 expression post-transcriptionally. Analysis of the addition and deletion of the second intron further indicated that it negatively controls SPF30 function. Our results highlight the critical role of SPF30 as a plant splicing factor involved in floral transition and propose a mechanism for the regulation of SPF30 itself via AS.
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Zhang et al. (2025) studied this question.
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