Arabidopsis PRMT5 Buffers Pre-mRNA Splicing and Development Against Genetic Variation in Donor Splice Sites
Genetic variation at splice site signals significantly influences alternative splicing, leading to transcriptomic and proteomic diversity that enhances phenotypic plasticity and adaptation. However, novel splice variants can negatively impact gene expression and developmental stability. Canalization—the ability of an organism to maintain a consistent phenotype despite genetic or environmental variations—helps balance the effects of genetic variation on development and evolution. Protein arginine methyltransferase 5 (PRMT5) is a key splicing regulator in plants and animals. Most splicing changes in prmt5 mutants are linked to weak donor splice sites, suggesting that PRMT5 may buffer splicing against genetic variation. We examined PRMT5's effects on splicing and development in two genetically divergent Arabidopsis thaliana accessions with different single nucleotide polymorphisms (SNPs) affecting donor splice sites. We found that PRMT5 inactivation significantly increased splicing and phenotypic differences between the accessions. Our findings suggest that PRMT5 contributes to canalization, mitigating the impact of splice site polymorphisms and facilitating the evolution of adaptive splicing patterns. Overall design: RNA-seq profiling of wild-type and prmt5-5 Arabidopsis thaliana plants belonging to Columbia and Landsberg accessions. RNA-seq profiling of wild-type and prmt5-5 F1 reciprocal hybrids of theses accessiones.