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Careno, D. A.

Publications and source records attributed to Careno, D. A..

2 recordsLinked to original sources

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 PRMT5s effects on splicing and development in two genetically divergent Arabidopsis thaliana accessions with different single nucleotide polymorphisms (SNPs) affecting donor splice sites. While PRMT5 inactivation similarly affected splicing in both backgrounds, it 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.

molecular biology↗

The 5'-3' exoribonuclease XRN4 modulates the plant circadian network in Arabidopsis

Circadian rhythms enable organisms to anticipate and adjust their physiology to periodic environmental changes. These rhythms are controlled by biological clocks that consist of a set of clock genes that regulate each other expression. Circadian oscillations in mRNA levels require regulation of mRNA production and degradation. While transcription factors controlling clock function have been well characterized from cyanobacteria to humans, the role of factors controlling mRNA decay is largely unknown. Here, we show that mutations in XRN4, the central component of the 5-3 mRNA decay pathway, alter clock function in Arabidopsis. We found that xrn4 mutants display long period phenotypes for clock gene expression and for the rhythm of leaf movement. These circadian defects were associated with changes in the circadian phases, but not overall mRNA levels, of several core clock genes. We then used non-invasive transcriptome-wide mRNA stability analysis to identify genes and pathways regulated by XRN4. Among genes affected in the xrn4 mutant at the transcriptional and post-transcriptional level, we found an enrichment in genes involved in auxin, ethylene, ABA signaling, and also circadian rhythmicity, although no significant effects were observed for canonical core-clock genes. Strikingly, the mRNAs of several clock regulated BBX genes were stabilized in xrn4 mutants. Some of these BBX genes are auxiliary factors controlling the pace of the clock and are candidates to mediate XRN4 effects on circadian period. Our results establish that, in Arabidopsis, the control of 5-3 mRNA decay by XRN4 constitutes a novel post-transcriptional regulatory layer of the circadian gene network.

plant biology↗