Wild strains of Arabidopsis (Arabidopsis thaliana) exhibit extensive natural variation in a wide variety of traits, including response to environmental changes. Ambient temperature is one of the major external factors that modulates plant growth and development. Here, we analyze the genetic architecture of natural variation in thermal responses of Arabidopsis. Exploiting wild accessions and recombinant inbred lines, we reveal extensive phenotypic variation in response to ambient temperature in distinct developmental traits such as hypocotyl elongation, root elongation, and flowering time. We show that variation in thermal response differs between traits, suggesting that the individual phenotypes do not capture all the variation associated with thermal response. Genome-wide association studies and quantitative trait locus analyses reveal that multiple rare alleles contribute to the genetic architecture of variation in thermal response. We identify at least 20 genomic regions that are associated with variation in thermal response. Further characterizations of temperature sensitivity quantitative trait loci that are shared between traits reveal a role for the blue-light receptor CRYPTOCHROME2 (CRY2) in thermosensory growth responses. We show the accession Cape Verde Islands is less sensitive to changes in ambient temperature, and through transgenic analysis, we demonstrate that allelic variation at CRY2 underlies this temperature insensitivity across several traits. Transgenic analyses suggest that the allelic effects of CRY2 on thermal response are dependent on genetic background suggestive of the presence of modifiers. In addition, our results indicate that complex light and temperature interactions, in a background-dependent manner, govern growth responses in Arabidopsis.Temperature is a critical environmental factor that has major effects on the growth, development, and distribution of plants across the globe (Fitter and Fitter, 2002;Samach and Wigge, 2005, 2013;Kotak et al., 2007;Penfield, 2008). With the predicted increase in global temperatures, and their potential impact on agricultural productivity, there are efforts to understand the genetic basis of temperature responses in plants. Traditionally, temperature effects have been studied in the context of extreme stress responses such as heat shock or cold shock (Kotak et al., 2007;Barrero-Gil and Salinas, 2013;Song et al., 2013;Storey and Storey, 2013). In recent times, there has been an interest in analyzing the response of plants to changes in their growth temperature within the nonstress range of l6°C to 27°C, as even small changes in temperature can have major impacts on plant growth and development (Wigge, 2013;Franklin et al., 2014). In this study, we refer to various phenotypic responses in plants that are attributable to small changes in ambient temperature as temperature/thermal response.A few specific phenotypic responses are often used to uncover the genetic and molecular basis of thermal response in plants. These include temperature-induced chan...

Transcriptional downregulation caused by intronic triplet repeat expansions underlies diseases such as Friedreich's ataxia. This downregulation of gene expression is coupled with epigenetic changes, but the underlying mechanisms are unknown. Here, we show that an intronic GAA/TTC triplet expansion within the IIL1 gene of Arabidopsis thaliana results in accumulation of 24-nt short interfering RNAs (siRNAs) and repressive histone marks at the IIL1 locus, which in turn causes its transcriptional downregulation and an associated phenotype. Knocking down DICER LIKE-3 (DCL3), which produces 24-nt siRNAs, suppressed transcriptional downregulation of IIL1 and the triplet expansion-associated phenotype. Furthermore, knocking down additional components of the RNA-dependent DNA methylation (RdDM) pathway also suppressed both transcriptional downregulation of IIL1 and the repeat expansion-associated phenotype. Thus, our results show that triplet repeat expansions can lead to local siRNA biogenesis, which in turn downregulates transcription through an RdDM-dependent epigenetic modification.

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