ArticlePlant physiology2025
The role of Arabidopsis Splicing Factor 30 in floral transition and the implications of its alternative splicing.
Article in Plant physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Splicing Factors in Plant Abiotic Stress Responses: Regulatory Mechanisms and Perspectives.Plants (Basel, Switzerland) · 2026Review
- The Role of Alternative Splicing in Polyploids in Response to Abiotic Stress.International journal of molecular sciences · 2025Review
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7 authors.
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Abstract
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 SPF30 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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