Project description:We report genome-wide transcriptional UV response in Deincoccus gobiensis Examination of the transcriptomes before and after UV irradiation in Deinococcus gobiensis
Project description:Plants use sunlight as a source of energy for photosynthesis but also as an important environmental cue to regulate growth, development and light acclimation. Wavelengths in the UV-B (280-315 nm) and UV-A/blue (315-500 nm) regions of the spectrum are perceived by UV RESISTANCE LOCUS 8 (UVR8) and cryptochromes (CRY1 and CRY2), respectively. Despite recent advances in our understanding of how these photoreceptors promote photomorphogenesis, very little is known about the molecular mechanisms regulated by UVR8 and CRYs in sunlight exposed plants. Here, a factorial experiment was designed to assess the roles of UVR8 and CRYs in regulating transcriptome wide changes, hormone accumulation, and growth competence of Arabidopsis thaliana plants exposed to solar UV-B, UV-A, and blue radiation.
Project description:Nucleotide excision repair is a primary DNA repair mechanism that removes bulky DNA adducts such as UV-induced pyrimidine dimers. Correspondingly, genome-wide mapping of nucleotide excision repair with eXcision Repair sequencing (XR-seq), provides comprehensive profiling of DNA damage repair. A number of XR-seq experiments at a variety of conditions for different damage types revealed heterogenous repair in the human genome. Although human repair profiles were extensively studied, how repair maps vary between primates is yet to be investigated. Here, we characterized the genome-wide UV-induced damage repair maps of the grey mouse lemur,Microcebus murinus, in comparison with human. We derived fibroblast cell lines from mouse lemur and exposed them to UV irradiation. Following repair events were captured genome-wide by XR-seq protocol 1 hour and 5 minutes after irradiation for cyclobutane pyrimidine dimers (CPD) and 6-4 pyrimidine-pyrimidone photoproducts ([6-4]PP), respectively. Mouse lemur repair profiles were analyzed in comparison with the equivalent human fibroblast datasets. We found that transcription-coupled repair levels for CPD repair differs between two primates. Despite this, comparative analysis of human and mouse lemur fibroblasts revealed that genome-wide repair profiles of the homologous regions between the primates are highly correlated. This correlation is stronger for the highly expressed genes as well as the genes sharing high homology. With the inclusion of an additional XR-seq sample derived from another human cell line in the analysis, we found that fibroblasts between two primates repair lesions more similarly relative to two distinct cell lines from human. These results suggest that mouse lemurs and humans, and possibly primates in general, share similar repair mechanism as well as genomic variance distribution.
Project description:UV radiation is a ubiquitous component of solar radiation that affects plant growth and development. Analysis of natural variation in response to UV radiation revealed significant differences among natural accessions of Arabidopsis thaliana. However, the genetic basis of this is to a large extent unknown. Here, we analyzed the response of Arabidopsis accessions to UV radiation stress by performing RNA-sequencing of three UV sensitive and three UV resistant accessions. The genome-wide transcriptional analysis revealed a large number of genes significantly up- or down-regulated only in sensitive or only in resistant accessions, respectively. Mutant analysis of few selected candidate genes suggested by the RNA-sequencing results indicate a connection between UV radiation stress and plant-pathogen-like defense responses.
Project description:We recently developed high-throughput sequencing approaches, eXcision Repair sequencing (XR-seq) and Damage-seq, to generate genome-wide mapping of DNA damage formation and excision repair, respectively, with single-nucleotide resolution. Here, we adopted time-course XR-seq data to profile UV-induced excision repair dynamics, paired with Damage-seq data to quantify the overall induced DNA damage. We identified genome-wide repair hotspots that are subject to exemplified amount of repair very soon after UV irradiation. We show that such repair hotspots do not result from hypersensitivity to DNA damage and are thus not damage hotspots. We find that the earliest repair occur preferentially in promoters and enhancers from open-chromatin regions. The repair hotspots are also significantly enriched for frequently interacting regions and super-enhancers, both of which are hotspots for local chromatin interactions. We further extend the interrogation of chromatin organization to DNA replication timing and conclude that early-repair hotspots are enriched for early-replication domains. Collectively, we report genome-wide early-repair hotspots of UV-induced damage, in association with chromatin states and epigenetic compartmentalization of the human genome.
Project description:UV radiation is a ubiquitous component of solar radiation that affects plant growth and development. Analysis of natural variation in response to UV radiation revealed significant differences among natural accessions of Arabidopsis thaliana. However, the genetic basis of this is to a large extent unknown. Here, we analyzed the response of Arabidopsis accessions to UV radiation stress by performing RNA-sequencing of three UV sensitive and three UV resistant accessions. The genome-wide transcriptional analysis revealed a large number of genes significantly up- or down-regulated only in sensitive or only in resistant accessions, respectively. Mutant analysis of few selected candidate genes suggested by the RNA-sequencing results indicate a connection between UV radiation stress and plant-pathogen-like defense responses. Examination of transcriptional changes in response to UV treatment in Arabidopsis natural accessions
Project description:We previously revealed developmental regulation over UV repair capacity in the soilborne pathogen Fusarium oxysporum (F. oxysporum). We demonstrated that photoreactivation assisted survival and repair were high during early stages of germination and low at later stages. In agreement, the expression of the UV specific repair genes photolyase and uvde showed opposite trends. While early on photolyase is induced and uvde is reduced, the trend is reversed later. Here, we tested the dynamic of transcription of photolyase, UV survival, repair capacity, and UV induced mutagenesis in the foliar pathogen Fusarium mangiferae. Unlike F. oxysporum, neither did we observe developmental control over photoreactivation dependent repair nor the changes in gene expression of phr1 and uvde throughout the experiment. Similarly, photo-reactivation assisted reduction in UV induced mutagenesis was similar throughout the development of F. mangiferae but fluctuated during the development of F. oxysporum. To generate hypotheses regarding the recovery of F. mangiferae after UV exposure, an RNAseq analysis was performed after irradiation at different timepoints. The most striking effect of UV on F. mangiferae was developmental-dependent induction of translation related genes. We further report a complex dynamic response that involves translation, cell cycle and lipid biology related genes.
Project description:We conducted transcript profiling and metabolome profiling induced by UV irradiation in grape berry skin. Transcriptome analysis was carried out with genome-wide microarray and two hundred thirty eight genes were more than 5-fold up-regulated by UV irradiation. The enrichment analysis showed GO terms including stilbene synthase (STS) gene. Moreover, the principal component analysis (PCA) of metabolome analysis showed a compound, identified resveratrol, accumulated in grape berry skin specifically. Our result clearly shows that UV irradiation induced only accumulation of resveratrol and its analogues but did not induce accumulation of the other phenolic compounds.