DNA Damage Atlas: an atlas of DNA damage and repair.

DNA damage and its improper repair are the major source of genomic alterations responsible for many human diseases, particularly cancer. To aid researchers in understanding the underlying mechanisms of genome instability, a number of genome-wide profiling approaches have been developed to monitor DNA damage and repair events. The rapid accumulation of published datasets underscores the critical necessity of a comprehensive database to curate sequencing data on DNA damage and repair intermediates. Here, we present DNA Damage Atlas (DDA, http://www.bioinformaticspa.com/DDA/), the first large-scale repository of DNA damage and repair information. Currently, DDA comprises 6,030 samples from 262 datasets by 59 technologies, covering 16 species, 10 types of damage and 135 treatments. Data collected in DDA was processed through a standardized workflow, including quality checks, hotspots identification and a series of feature characterization for the hotspots. Notably, DDA encompasses analyses of highly repetitive regions, ribosomal DNA and telomere. DDA offers a user-friendly interface that facilitates browsing, searching, genome browser visualization, hotspots comparison and data downloading, enabling convenient and thorough exploration for datasets of interest. In summary, DDA will stand as a valuable resource for research in genome instability and its association with diseases.

The H3K9me2-binding protein AGDP3 limits DNA methylation and transcriptional gene silencing in Arabidopsis.

DNA methylation, a conserved epigenetic mark, is critical for tuning temporal and spatial gene expression. The Arabidopsis thaliana DNA glycosylase/lyase REPRESSOR OF SILENCING 1 (ROS1) initiates active DNA demethylation and is required to prevent DNA hypermethylation at thousands of genomic loci. However, how ROS1 is recruited to specific loci is not well understood. Here, we report the discovery of Arabidopsis AGENET Domain Containing Protein 3 (AGDP3) as a cellular factor that is required to prevent gene silencing and DNA hypermethylation. AGDP3 binds to H3K9me2 marks in its target DNA via its AGD12 cassette. Analysis of the crystal structure of the AGD12 cassette of AGDP3 in complex with an H3K9me2 peptide revealed that dimethylated H3K9 and unmodified H3K4 are specifically anchored into two different surface pockets. A histidine residue located in the methyllysine binding aromatic cage provides AGDP3 with pH-dependent H3K9me2 binding capacity. Our results uncover a molecular mechanism for the regulation of DNA demethylation by the gene silencing mark H3K9me2.

SIN3 LIKE genes mediate long-day induction of flowering but inhibit the floral transition in short days through histone deacetylation in Arabidopsis.

Day length or photoperiod changes are crucial for plants to align the timing of the floral transition with seasonal changes. Through the photoperiod pathway, day length changes induce the expression of the florigenic FLOWERING LOCUS T (FT) to promote flowering. In the facultative long days (LDs) plant Arabidopsis thaliana, LD signals induce flowering, whereas short days (SDs) inhibit flowering. Here, we show that in Arabidopsis SIN3 LIKE (SNL) family genes, encoding a scaffold protein for assembly of histone deacetylase complexes, directly repress the expression of an FT activator and three FT repressors to regulate the transition to flowering in SDs and LDs, respectively. Under inductive LDs, SNLs including SIN3 LIKE 1 (SNL1) to SNL5, function in partial redundancy to repress the expression of three AP2 family transcription factors that repress FT expression, and therefore mediate LD induction of FT expression and promote the transition to flowering. In contrast, under non-inductive SDs SNLs act to inhibit the floral transition, partly through direct repression of a MADS box transcriptional factor that promotes FT expression. Therefore, our results reveal that SNLs, through histone deacetylation, play a dual role for the control of flowering in the LD plant Arabidopsis: inhibiting flowering when the day length is shorter and promoting the floral transition when days become longer than a threshold length.

Cassava genetic transformation and its application in breeding.

As a major source of food, cassava (Manihot esculenta Crantz) is an important root crop in the tropics and subtropics of Africa and Latin America, and serves as raw material for the production of starches and bioethanol in tropical Asia. Cassava improvement through genetic engineering not only overcomes the high heterozygosity and serious trait separation that occurs in its traditional breeding, but also quickly achieves improved target traits. Since the first report on genetic transformation in cassava in 1996, the technology has gradually matured over almost 15 years of development and has overcome cassava genotype constraints, changing from mode cultivars to farmer-preferred ones. Significant progress has been made in terms of an increased resistance to pests and diseases, biofortification, and improved starch quality, building on the fundamental knowledge and technologies related to planting, nutrition, and the processing of this important food crop that has often been neglected. Therefore, cassava has great potential in food security and bioenergy development worldwide.

SWO1 modulates cell wall integrity under salt stress by interacting with importin ɑ in Arabidopsis.

Maintenance of cell wall integrity is of great importance not only for plant growth and development, but also for the adaptation of plants to adverse environments. However, how the cell wall integrity is modulated under salt stress is still poorly understood. Here, we report that a nuclear-localized Agenet domain-containing protein SWO1 (SWOLLEN 1) is required for the maintenance of cell wall integrity in Arabidopsis under salt stress. Mutation in SWO1 gene results in swollen root tips, disordered root cell morphology, and root elongation inhibition under salt stress. The swo1 mutant accumulates less cellulose and pectin but more lignin under high salinity. RNA-seq and ChIP-seq assays reveal that SWO1 binds to the promoter of several cell wall-related genes and regulates their expression under saline conditions. Further study indicates that SWO1 interacts with importin ɑ IMPA1 and IMPA2, which are required for the import of nuclear-localized proteins. The impa1 impa2 double mutant also exhibits root growth inhibition under salt stress and mutations of these two genes aggravate the salt-hypersensitive phenotype of the swo1 mutant. Taken together, our data suggest that SWO1 functions together with importin ɑ to regulate the expression of cell wall-related genes, which enables plants to maintain cell wall integrity under high salinity.