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Cell-cycle checkpoints and DNA repair processes protect organisms from potentially lethal mutational damage. Compared to other budding yeasts in the subphylum Saccharomycotina, we noticed that a lineage in the genus Hanseniaspora exhibited very high evolutionary rates, low Guanine-Cytosine (GC) content, small genome sizes, and lower gene numbers. To better understand Hanseniaspora evolution, we analyzed 25 genomes, including 11 newly sequenced, representing 18/21 known species in the genus. Our phylogenomic analyses identify two Hanseniaspora lineages, a faster-evolving lineage (FEL), which began diversifying approximately 87 million years ago (mya), and a slower-evolving lineage (SEL), which began diversifying approximately 54 mya. Remarkably, both lineages lost genes associated with the cell cycle and genome integrity, but these losses were greater in the FEL. E.g., all species lost the cell-cycle regulator WHIskey 5 (WHI5), and the FEL lost components of the spindle checkpoint pathway (e.g., Mitotic Arrest-Deficient 1 [MAD1], Mitotic Arrest-Deficient 2 [MAD2]) and DNA-damage-checkpoint pathway (e.g., Mitosis Entry Checkpoint 3 [MEC3], RADiation sensitive 9 [RAD9]). Similarly, both lineages lost genes involved in DNA repair pathways, including the DNA glycosylase gene 3-MethylAdenine DNA Glycosylase 1 (MAG1), which is part of the base-excision repair pathway, and the DNA photolyase gene PHotoreactivation Repair deficient 1 (PHR1), which is involved in pyrimidine dimer repair. Strikingly, the FEL lost 33 additional genes, including polymerases (i.e., POLymerase 4 [POL4] and POL32) and telomere-associated genes (e.g., Repressor/activator site binding protein-Interacting Factor 1 [RIF1], Replication Factor A 3 [RFA3], Cell Division Cycle 13 [CDC13], Pbp1p Binding Protein [PBP2]). Echoing these losses, molecular evolutionary analyses reveal that, compared to the SEL, the FEL stem lineage underwent a burst of accelerated evolution, which resulted in greater mutational loads, homopolymer instabilities, and higher fractions of mutations associated with the common endogenously damaged base, 8-oxoguanine. We conclude that Hanseniaspora is an ancient lineage that has diversified and thrived, despite lacking many otherwise highly conserved cell-cycle and genome integrity genes and pathways, and may represent a novel, to our knowledge, system for studying cellular life without them.

DNA damage is generated by various environmental stressors and so DNA repair systems must inevitably adapt to changing environments. Photolyases represent a highly conserved class of enzymes which repair UV-induced covalent crosslinks between adjacent pyrimidine bases (CPD and 6-4 photoproducts) via photoreactivation. In the blind cavefish Phreatichthys andruzzii which has evolved for millions of years completely isolated from UV radiation and visible light, we have documented multiple polymorphisms and loss of function mutations affecting both the 6-4phr and DASHphr photolyase genes while strangely, the CPDphr gene remains highly conserved. Using loss and gain of photolyase function medaka and mammalian cell lines, we reveal a novel function for CPDphr. Specifically, it enables the light-independent repair of CPD as well as 8-OHdG, an oxidatively modified form of guanosine which are both generated under oxidative stress in the absence of UV radiation. Thereby we document selective conservation of light-independent photolyase function in blind cavefish, enabling the repair of DNA damage encountered in an extreme subterranean environment. By investigating the paradoxical retention of a photolyase gene in a light-deprived blind cavefish, the authors reveal a novel light-independent function for CPD photolyase in the repair of oxidative stress-induced DNA damage

Dysregulated sleep has widespread health consequences, including the accumulation of DNA damage. The Mexican tetra, Astyanax mexicanus , provides a powerful model to study the evolution and consequences of sleep loss. Multiple cave-adapted populations of this species have independently evolved reduced sleep compared to surface populations, yet show no obvious decline in healthspan or longevity. To examine whether evolved sleep loss is associated with DNA damage, we compared DNA damage response (DDR) and oxidative stress across populations. Cavefish exhibited elevated γH2AX in the brain and increased gut oxidative stress, consistent with chronic sleep deprivation. Following acute UV exposure, surface fish, but not cavefish, increased sleep and activated the photoreactivation repair pathway. Fibroblast cell lines derived from both populations confirmed diminished DDR and repair in cavefish, supporting an attenuated acute DNA damage response. Transcriptomic analysis revealed that many genes differentially expressed with aging in surface fish remain unchanged in cavefish, suggesting altered regulation of aging-related pathways. Together, these findings indicate that cavefish experience elevated cellular hallmarks of sleep deprivation yet exhibit resilience to its long-term consequences, highlighting an evolutionary model to investigate the mechanisms underlying sleep, DNA repair, and healthy aging.

Ultraviolet (UV) light-emitting diodes (LEDs) have emerged as a promising technology for water disinfection, offering selectable wavelengths that enable more precise targeting of specific cellular components. This study evaluated the inactivation efficiency of water quality indicators with different cell morphologies and envelope organization, Escherichia coli (Gram-negative) and Enterococcus faecium (Gram-positive), including both environmental and culture collection strains, using UV-C LEDs that emit light at 255 nm, 260 nm, 265 nm, 270 nm, and 280 nm. Inactivation kinetics as well as post-exposure repair, under dark and light conditions, were evaluated. Fluorescence microscopy observations and cyclobutane pyrimidine dimer formation were analyzed to elucidate morphological changes and DNA damage. Within the tested range, 265 nm LEDs achieved the highest inactivation rates for E. coli at a given UV fluence, consistent with the DNA absorption maximum in the 260–270 nm region. In contrast, E. faecium showed similar inactivation between 260 and 270 nm. Nevertheless, all tested wavelengths demonstrated high efficacy, achieving up to 6-log inactivation of both culture collection and environmental strains at low UV fluences (below 7 mJ/cm²). E. faecium showed enhanced resilience at lower fluences for all the wavelengths tested. Fluorescence microscopy revealed that both membrane integrity and DNA structure were increasingly affected by higher UV fluences, although signs of DNA damage were more pronounced and detectable even at lower exposure levels. Additionally, none of the strains tested showed considerable photoreactivation or dark repair capability, implying that the induced DNA lesions were largely irreversible under our experimental conditions. This study shows the efficacy of UV-C LEDs for water disinfection across a range of wavelengths, particularly at 265 nm, highlighting the important contribution of DNA damage to bacterial inactivation, and emphasizing their applicability for the water industry.

Ultraviolet (UV) component of solar radiation impairs genome stability by inducing the formation of pyrimidine-pyrimidone (6-4) photoproducts [(6-4)PPs] in plant genomes. (6-4)PPs disrupt growth and development by interfering with transcription and DNA replication. To resist UV stress, plants employ both photoreactivation and nucleotide excision repair that excises oligonucleotide containing (6-4)PPs through two subpathways: global and transcription-coupled excision repair (TCR). Here, we analyzed the genome-wide excision repair-mediated repair of (6-4)PPs in Arabidopsis thaliana and found that (6-4)PPs can be repaired by TCR; however, the main subpathway to remove (6-4)PPs from the genome is global repair. Our analysis showed that open chromatin genome regions are more rapidly repaired than heterochromatin regions, and the repair level peaks at the promoter, transcription start site and transcription end site of genes. Our study revealed that the repair of (6-4)PP in plants showed a distinct genome-wide repair profile compared to the repair of other major UV-induced DNA lesion called cyclobutane pyrimidine dimers (CPDs).

Ultraviolet disinfection is an important method for controlling the large-scale outbreaks of diseases in aquaculture. As a novel and promising light source, ultraviolet light-emitting diode (UV-LED) has the advantages of safety, high efficiency and no environmental pollution risks. However, it remains unclear whether UV-LEDs can replace traditional UV light sources for aquaculture water treatment processes. Present study aimed to investigate the efficacy of UVC-LEDs (265 nm) on pathogenic bacteria, specifically Aeromonas salmonicida and Escherichia coli . The effects of UVC-LED dose, light conditions, and temperature on bacterial reactivation were also investigated. The results showed that exposure to UVC-LED effectively inactivated both types of bacteria. To achieve 4.5-log inactivation of A. salmonicida and E. coli , 24 mJ/cm 2 and 28 mJ/cm 2 UVC-LED irradiation were required, and the inactivation rate increased with increasing UVC-LED fluence. Both A. salmonicida and E. coli were revived after UVC-LED disinfection, and photoreactivation was significantly higher than dark reactivation. Bacterial reactivation rate due to high-dose UVC-LED treatment was significantly lower than that of low-dose. After 72 h of reactivation, photoreactivation and dark reactivation rates were 1 ± 0.4% and 2.2 ± 0.2%for A. salmonicida , and 0.02% and 0% for E. coli , respectively. Besides, the photoreactivation rates for the two bacteria exhibited different correlations with temperature. The highest photoreactivation rate for A. salmonicida was 68.7 ± 4% at 20°C, while the highest photoreactivation rate for E. coli was 53.98 ± 2.9% at 15°C for 48 h. This study reveals the rapid and efficient inactivation of bacteria by UVC-LED, and elucidates the mechanism and influencing factors for inactivation and reactivation by UVC-LED. The study also highlights that adequate UVC-LED irradiation and avoidance of visible light after UVC-LED disinfection can effectively inhibit bacterial reactivation. Our findings form a reference for the design and operation of UV disinfection in aquaculture.

Although solar light is indispensable for the functioning of plants, this environmental factor may also cause damage to living cells. Apart from the visible range, including wavelengths used in photosynthesis, the ultraviolet (UV) light present in solar irradiation reaches the Earth’s surface. The high energy of UV causes damage to many cellular components, with DNA as one of the targets. Putting together the puzzle-like elements responsible for the repair of UV-induced DNA damage is of special importance in understanding how plants ensure the stability of their genomes between generations. In this review, we have presented the information on DNA damage produced under UV with a special focus on the pyrimidine dimers formed between the neighboring pyrimidines in a DNA strand. These dimers are highly mutagenic and cytotoxic, thus their repair is essential for the maintenance of suitable genetic information. In prokaryotic and eukaryotic cells, with the exception of placental mammals, this is achieved by means of highly efficient photorepair, dependent on blue/UVA light, which is performed by specialized enzymes known as photolyases. Photolyase properties, as well as their structure, specificity and action mechanism, have been briefly discussed in this paper. Additionally, the main gaps in our knowledge on the functioning of light repair in plant organelles, its regulation and its interaction between different DNA repair systems in plants have been highlighted.

Many environmental microorganisms live in constant balance between UV damage and repair. The simplest repair process called photoreactivation starts immediately when microbial cells face sunlight irradiation. The aim of the study is to assess the ability of bacteria, virus, and mould suspended in the air and deposited on different surfaces to photoreactivation after their exposure to UV-C radiation produced by two disinfection devices, i.e. low-pressure mercury lamp (LPML) and light-emitting diodes (LEDs). Five microbial strains ( ATCC 6538, ATCC 6633, ATCC 260, ATCC 9577, and bacteriophage PhiX174 ATCC 13706-B1) deposited on metal, plastic, and glass surfaces, as well as dispersed in the air as bioaerosols, were irradiated with high UV-C doses (762 J/m and 832 J/m ), and subsequently exposed for 24 h to visible light with a wide (380-780 nm) spectral range to check their ability to photorecovery. UV-C radiation emitted by LPML and LEDs effectively inactivated the tested microorganisms deposited on metal, plastic and glass surfaces, as well as dispersed in the air. However, this type of inactivation is not an irreversible process and subsequent exposure of microbiologically contaminated elements of the environment with visible light may partially rebuild the population of pathogenic microorganisms in photoreactivation process. Effective cleaning of both the surfaces and air cannot be limited to their exposure to UV-C radiation, but should be supplemented with other techniques for neutralizing microorganisms, which need be subsequently applied after such exposure.

Ultraviolet (UV) radiation is one of the most genotoxic, universal agents present in the environment. UVB (280-315 nm) radiation directly damages DNA, producing cyclobutane pyrimidine dimers (CPDs) and pyrimidine 6-4 pyrimidone photoproducts (6-4PPs). These photolesions interfere with essential cellular processes by blocking transcription and replication polymerases, and may induce skin inflammation, hyperplasia and cell death eventually contributing to skin aging, effects mediated mainly by keratinocytes. Additionally, these lesions may also induce mutations and thereby cause skin cancer. Photolesions are repaired by the Nucleotide Excision Repair (NER) pathway, responsible for repairing bulky DNA lesions. Both types of photolesions can also be repaired by distinct (CPD- or 6-4PP-) photolyases, enzymes that specifically repair their respective photolesion by directly splitting each dimer through a light-dependent process termed photoreactivation. However, as photolyases are absent in placental mammals, these organisms depend solely on NER for the repair of DNA UV lesions. However, the individual contribution of each UV dimer in the skin effects, as well as the role of keratinocytes has remained elusive. In this study, we show that in NER-deficient mice, the transgenic expression and photorepair of CPD-photolyase in basal keratinocytes completely inhibited UVB-induced epidermal thickness and cell proliferation. On the other hand, photorepair by 6-4PP-photolyase in keratinocytes reduced but did not abrogate these UV-induced effects. The photolyase mediated removal of either CPDs or 6-4PPs from basal keratinocytes in the skin also reduced UVB-induced apoptosis, ICAM-1 expression, and myeloperoxidase activation. These findings indicate that, in NER-deficient rodents, both types of photolesions have causal roles in UVB-induced epidermal cell proliferation, hyperplasia, cell death and inflammation. Furthermore, these findings also support the notion that basal keratinocytes, instead of other skin cells, are the major cellular mediators of these UVB-induced effects.

We have gained considerable insight into the mechanisms which recognize and repair DNA damage, but how they adapt to extreme environmental challenges remains poorly understood. Cavefish have proven to be fascinating models for exploring the evolution of DNA repair in the complete absence of UV-induced DNA damage and light. We have previously revealed that the Somalian cavefish Phreatichthys andruzzii , lacks photoreactivation repair via the loss of light, UV and ROS-induced photolyase gene transcription mediated by D-box enhancer elements. Here, we explore whether other systems repairing UV-induced DNA damage have been similarly affected in this cavefish model. By performing a comparative study using P . andruzzii and the surface-dwelling zebrafish, we provide evidence for a conservation of sunlight-regulated Nucleotide Excision Repair (NER). Specifically, the expression of the ddb2 gene which encodes a key NER recognition factor is robustly induced following exposure to light, UV and oxidative stress in both species. As in the case of the photolyase genes, D-boxes in the ddb2 promoter are sufficient to induce transcription in zebrafish. Interestingly, despite the loss of D-box-regulated photolyase gene expression in P . andruzzii , the D-box is required for ddb2 induction by visible light and oxidative stress in cavefish. However, in the cavefish ddb2 gene this D-box-mediated induction requires cooperation with an adjacent, highly conserved E2F element. Furthermore, while in zebrafish UV-induced ddb2 expression results from transcriptional activation accompanied by stabilization of the ddb2 mRNA, in P . andruzzii UV induces ddb2 expression exclusively via an increase in mRNA stability. Thus, we reveal plasticity in the transcriptional and post transcriptional mechanisms regulating the repair of sunlight-induced DNA damage under long-term environmental challenges.