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Biology subjects

Sieburth, L. E.

Publications and source records attributed to Sieburth, L. E..

3 recordsLinked to original sources

Neighboring codon adjacent nucleotides have a conserved influence on mRNA decay

BackgroundDegeneracy in the genetic code has been shown to play a major role in yeast mRNA stability; differences in optimality (charged tRNA supply vs demand) among synonymous codons were revealed as a determinant of mRNA decay rates. However, whether and how much this mechanism determines mRNA decay rates in plants is unsettled. Furthermore, whether factors other than charged tRNA abundance influence codon optimality remains unexplored. ResultsHere, biased codon usage in Arabidopsis correlated with mRNA decay rates. A codon-optimality model of mRNA decay rate based on codon frequencies was tested using synonymously recoded genes. mRNA decay rates of these alleles in transgenic plants was consistent with the model predictions. Arabidopsis appears to use the same mechanism for sensing low optimality codons as yeast and humans because the N-terminal sensor domain of NOT3 is conserved. However, decay rates were also affected by codon context. Neighboring codons adjacent nucleotides consistently shifted codon correlations with decay rate in Arabidopsis, which was also observed in other published datasets revealing an influence of codon sequence on translation that is independent of charged tRNA concentrations. ConclusionsCodons frequencies explained 21% of decay rate variance, suggesting codon optimality-mediated decay is one of multiple mechanisms that determine decay rates in plants. Our study also found codon context as an additional factor that affects mRNA stability and establishes a paradigm of selection among synonymous codons decoded through wobble base pairing.

genomics↗

RNA decay regulates RNA abundances and transcriptome homeostasis using different mechanisms

RNA decay is essential for maintenance of normal RNA abundances; however how RNA decay is regulated to contribute to changes in RNA abundances is poorly understood. Here, we addressed this question by analyzing rates of RNA abundance change, RNA half- lives (t1/2s), and transcription rates in stimulated Arabidopsis leaf cells. This revealed three mechanisms by which decay influenced RNA abundance changes. First, the biggest changes in RNA abundances resulted from t1/2 changes that reinforced transcriptional regulation (synergistic). Modest RNA abundance changes arose from a second mechanism in which t1/2 changes opposed transcriptional regulation (oppositional). Finally, RNA decay alone also contributed to RNA abundance change, and RNA decays measured capacity influence RNA abundances was similar to that of transcription. RNA decay also contributed to transcriptome homeostasis through stimulus-induced RNA buffering. Oppositional and buffering regulation shared key features, including excessive and commensurate rate changes, which suggested use of a shared regulatory mechanism which we call countercyclical regulation. In this study, countercyclical regulation was widespread and used for regulation of 90% of the RNAs with t1/2 regulation.

molecular biology↗

DHH1/DDX6-like RNA helicases maintain ephemeral half-lives of stress-response mRNAs associated with innate immunity and growth inhibition

Gene transcription is counterbalanced by mRNA decay processes that regulate transcript quality and quantity. We show here that the evolutionarily conserved DHH1/DDX6-like RNA HELICASEs of Arabidopsis thaliana control the ephemerality of a subset of cellular mRNAs. These RNA helicases co-localize with key markers of processing bodies and stress granules and contribute to their subcellular dynamics. These RHs function to limit the precocious accumulation and translation of stress-responsive mRNAs associated with autoimmunity and growth inhibition under non-stress conditions. Given the conservation of this RH subfamily, they may control basal levels of conditionally-regulated mRNAs in diverse eukaryotes, accelerating responses without penalty.

plant biology↗