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Karine Van Doninck - One of the best experts on this subject based on the ideXlab platform.
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gateway to genetic exchange dna double strand breaks in the bdelloid rotifer adineta Vaga submitted to desiccation
Journal of Evolutionary Biology, 2014Co-Authors: Boris Hespeels, M Knapen, D Hanotmambres, Annecatherine Heuskin, F Pineux, Stephane Lucas, Romain Koszul, Karine Van DoninckAbstract:: The bdelloid rotifer lineage Adineta Vaga inhabits temporary habitats subjected to frequent episodes of drought. The recently published draft sequence of the genome of A. Vaga revealed a peculiar genomic structure incompatible with meiosis and suggesting that DNA damage induced by desiccation may have reshaped the genomic structure of these organisms. However, the causative link between DNA damage and desiccation has never been proven to date in rotifers. To test for the hypothesis that desiccation induces DNA double-strand breaks (DSBs), we developed a protocol allowing a high survival rate of desiccated A. Vaga. Using pulsed-field gel electrophoresis to monitor genomic integrity, we followed the occurrence of DSBs in dried bdelloids and observed an accumulation of these breaks with time spent in dehydrated state. These DSBs are gradually repaired upon rehydration. Even when the genome was entirely shattered into small DNA fragments by proton radiation, A. Vaga individuals were able to efficiently recover from desiccation and repair a large amount of DSBs. Interestingly, when investigating the influence of UV-A and UV-B exposure on the genomic integrity of desiccated bdelloids, we observed that these natural radiations also caused important DNA DSBs, suggesting that the genome is not protected during the desiccated stage but that the repair mechanisms are extremely efficient in these intriguing organisms.
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gateway to genetic exchange dna double strand breaks in the bdelloid rotifer adineta Vaga submitted to desiccation
Journal of Evolutionary Biology, 2014Co-Authors: Boris Hespeels, M Knapen, D Hanotmambres, Annecatherine Heuskin, F Pineux, Stephane Lucas, Romain Koszul, Karine Van DoninckAbstract:: The bdelloid rotifer lineage Adineta Vaga inhabits temporary habitats subjected to frequent episodes of drought. The recently published draft sequence of the genome of A. Vaga revealed a peculiar genomic structure incompatible with meiosis and suggesting that DNA damage induced by desiccation may have reshaped the genomic structure of these organisms. However, the causative link between DNA damage and desiccation has never been proven to date in rotifers. To test for the hypothesis that desiccation induces DNA double-strand breaks (DSBs), we developed a protocol allowing a high survival rate of desiccated A. Vaga. Using pulsed-field gel electrophoresis to monitor genomic integrity, we followed the occurrence of DSBs in dried bdelloids and observed an accumulation of these breaks with time spent in dehydrated state. These DSBs are gradually repaired upon rehydration. Even when the genome was entirely shattered into small DNA fragments by proton radiation, A. Vaga individuals were able to efficiently recover from desiccation and repair a large amount of DSBs. Interestingly, when investigating the influence of UV-A and UV-B exposure on the genomic integrity of desiccated bdelloids, we observed that these natural radiations also caused important DNA DSBs, suggesting that the genome is not protected during the desiccated stage but that the repair mechanisms are extremely efficient in these intriguing organisms.
Romain Koszul - One of the best experts on this subject based on the ideXlab platform.
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gateway to genetic exchange dna double strand breaks in the bdelloid rotifer adineta Vaga submitted to desiccation
Journal of Evolutionary Biology, 2014Co-Authors: Boris Hespeels, M Knapen, D Hanotmambres, Annecatherine Heuskin, F Pineux, Stephane Lucas, Romain Koszul, Karine Van DoninckAbstract:: The bdelloid rotifer lineage Adineta Vaga inhabits temporary habitats subjected to frequent episodes of drought. The recently published draft sequence of the genome of A. Vaga revealed a peculiar genomic structure incompatible with meiosis and suggesting that DNA damage induced by desiccation may have reshaped the genomic structure of these organisms. However, the causative link between DNA damage and desiccation has never been proven to date in rotifers. To test for the hypothesis that desiccation induces DNA double-strand breaks (DSBs), we developed a protocol allowing a high survival rate of desiccated A. Vaga. Using pulsed-field gel electrophoresis to monitor genomic integrity, we followed the occurrence of DSBs in dried bdelloids and observed an accumulation of these breaks with time spent in dehydrated state. These DSBs are gradually repaired upon rehydration. Even when the genome was entirely shattered into small DNA fragments by proton radiation, A. Vaga individuals were able to efficiently recover from desiccation and repair a large amount of DSBs. Interestingly, when investigating the influence of UV-A and UV-B exposure on the genomic integrity of desiccated bdelloids, we observed that these natural radiations also caused important DNA DSBs, suggesting that the genome is not protected during the desiccated stage but that the repair mechanisms are extremely efficient in these intriguing organisms.
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gateway to genetic exchange dna double strand breaks in the bdelloid rotifer adineta Vaga submitted to desiccation
Journal of Evolutionary Biology, 2014Co-Authors: Boris Hespeels, M Knapen, D Hanotmambres, Annecatherine Heuskin, F Pineux, Stephane Lucas, Romain Koszul, Karine Van DoninckAbstract:: The bdelloid rotifer lineage Adineta Vaga inhabits temporary habitats subjected to frequent episodes of drought. The recently published draft sequence of the genome of A. Vaga revealed a peculiar genomic structure incompatible with meiosis and suggesting that DNA damage induced by desiccation may have reshaped the genomic structure of these organisms. However, the causative link between DNA damage and desiccation has never been proven to date in rotifers. To test for the hypothesis that desiccation induces DNA double-strand breaks (DSBs), we developed a protocol allowing a high survival rate of desiccated A. Vaga. Using pulsed-field gel electrophoresis to monitor genomic integrity, we followed the occurrence of DSBs in dried bdelloids and observed an accumulation of these breaks with time spent in dehydrated state. These DSBs are gradually repaired upon rehydration. Even when the genome was entirely shattered into small DNA fragments by proton radiation, A. Vaga individuals were able to efficiently recover from desiccation and repair a large amount of DSBs. Interestingly, when investigating the influence of UV-A and UV-B exposure on the genomic integrity of desiccated bdelloids, we observed that these natural radiations also caused important DNA DSBs, suggesting that the genome is not protected during the desiccated stage but that the repair mechanisms are extremely efficient in these intriguing organisms.
Yoshio Yamaoka - One of the best experts on this subject based on the ideXlab platform.
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Role of vacuolating cytotoxin A in Helicobacter pylori infection and its impact on gastric pathogenesis
'Informa UK Limited', 2020Co-Authors: Shamshul Ansari, Yoshio YamaokaAbstract:causes, via the influence of several virulence factors, persistent infection of the stomach, which leads to severe complications. Vacuolating cytotoxin A (VacA) is observed in almost all clinical strains of H. pylori; however, only some strains produce the toxigenic and pathogenic VacA, which is influenced by the gene sequence variations. VacA exerts its action by causing cell vacuolation and apoptosis. We performed a PubMed search to review the latest literatures published in English language. Areas covered Articles regarding H. pylori VacA and its genotypes, architecture, internalization, and role in gastric infection and pathogenicity are reviewed. We included the search for recently published literature until January 2020. Expert opinion H. pylori VacA plays a crucial role in severe gastric pathogenicity. In addition, VacA mediated in vivo bacterial survival leads to persistent infection and an enhanced bacterial evasion from the action of antibiotics and the innate host defense system, which leads to drug evasion. VacA as a co-stimulator for the CagA phosphorylation may exert a synergistic effect playing an important role in the CagA-mediated pathogenicity
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helicobacter pylori vaca acting through receptor protein tyrosine phosphatase α is crucial for caga phosphorylation in human duodenum carcinoma cell line az 521
Disease Models & Mechanisms, 2016Co-Authors: Masayuki Nakano, Yoshio Yamaoka, Kinnosuke Yahiro, Eiki Yamasaki, Hisao Kurazono, Junko Akada, Takuro Niidome, Masanori Hatakeyama, Hidekazu SuzukiAbstract:Helicobacter pylori, a major cause of gastroduodenal diseases, produces vacuolating cytotoxin (VacA) and cytotoxin-associated gene A (CagA), which seem to be involved in virulence. VacA exhibits pleiotropic actions in gastroduodenal disorders via its specific receptors. Recently, we found that VacA induced the phosphorylation of cellular Src kinase (Src) at Tyr418 in AZ-521 cells. Silencing of receptor protein tyrosine phosphatase (RPTP)α, a VacA receptor, reduced VacA-induced Src phosphorylation. Src is responsible for tyrosine phosphorylation of CagA at its Glu-Pro-Ile-Tyr-Ala (EPIYA) variant C (EPIYA-C) motif in Helicobacter pylori-infected gastric epithelial cells, resulting in binding of CagA to SHP-2 phosphatase. Challenging AZ-521 cells with wild-type H. pylori induced phosphorylation of CagA, but this did not occur when challenged with a vacA gene-disrupted mutant strain. CagA phosphorylation was observed in cells infected with a vacA gene-disrupted mutant strain after addition of purified VacA, suggesting that VacA is required for H. pylori-induced CagA phosphorylation. Following siRNA-mediated RPTPα knockdown in AZ-521 cells, infection with wild-type H. pylori and treatment with VacA did not induce CagA phosphorylation. Taken together, these results support our conclusion that VacA mediates CagA phosphorylation through RPTPα in AZ-521 cells. These data indicate the possibility that Src phosphorylation induced by VacA is mediated through RPTPα, resulting in activation of Src, leading to CagA phosphorylation at Tyr972 in AZ-521 cells.
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mechanisms of disease helicobacter pylori virulence factors
Nature Reviews Gastroenterology & Hepatology, 2010Co-Authors: Yoshio YamaokaAbstract:Helicobacter pylori has an essential role in the development of various gastroduodenal diseases, but only a small proportion of people infected with H. pylori develop these diseases. In this Review, Yoshio Yamaoka discusses current knowledge of the H. pylori virulence factors CagA, VacA, OipA and DupA. In particular, he considers how these virulence factors contribute to differing geographic gastric cancer disease patterns and to the development of both gastric cancer and duodenal ulcer.
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disease association with two helicobacter pylori duplicate outer membrane protein genes homb and homa
Gut Pathogens, 2009Co-Authors: Monica Oleastro, Francis Mégraud, Dulciene M M Queiroz, Yoshio Yamaoka, Rita Cordeiro, Lurdes Monteiro, Armelle MenardAbstract:Background homB encodes a Helicobacter pylori outer membrane protein. This gene was previously associated with peptic ulcer disease (PUD) and was shown to induce activation of interleukin-8 secretion in vitro, as well as contributing to bacterial adherence. Its 90%-similar gene, homA, was previously correlated with gastritis. The present study aimed to evaluate the gastric disease association with homB and homA, as well as with the H. pylori virulence factors cagA, babA and vacA, in 415 H. pylori strains isolated from patients from East Asian and Western countries. The correlation among these genotypes was also evaluated.
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regulation of gastric carcinogenesis by helicobacter pylori virulence factors
Cancer Research, 2008Co-Authors: Aime T Franco, Yoshio Yamaoka, Elizabeth Johnston, Uma Krishna, Dawn A Israel, Toni A Nagy, Lydia E Wroblewski, Maria Blanca Piazuelo, Pelayo Correa, Richard M PeekAbstract:Helicobacter pylori is the strongest known risk factor for gastric adenocarcinoma, and strains that possess the cag secretion system, which translocates the bacterial effector CagA into host cells, augment cancer risk. H. pylori strains that express the vacuolating cytotoxin or the outer membrane protein OipA are similarly associated with severe pathologic outcomes. We previously reported that an in vivo adapted H. pylori strain, 7.13, induces gastric adenocarcinoma in rodent models of gastritis. In the current study, we used carcinogenic strain 7.13 as a prototype to define the role of virulence constituents in H. pylori-mediated carcinogenesis. Mongolian gerbils were infected with wild-type strain 7.13 or cagA(-), vacA(-), or oipA(-) mutants for 12 to 52 weeks. All infected gerbils developed gastritis; however, inflammation was significantly attenuated in animals infected with the cagA(-) but not the vacA(-) or oipA(-) strains. Gastric dysplasia and cancer developed in >50% of gerbils infected with either the wild-type or vacA(-) strain but in none of the animals infected with the cagA(-) strain. Inactivation of oipA decreased beta-catenin nuclear localization in vitro and reduced the incidence of cancer in gerbils. OipA expression was detected significantly more frequently among H. pylori strains isolated from human subjects with gastric cancer precursor lesions versus persons with gastritis alone. These results indicate that loss of CagA prevents the development of cancer in this model. Inactivation of oipA attenuates beta-catenin nuclear translocation and also decreases the incidence of carcinoma. In addition to defining factors that mediate H. pylori-induced cancer, these results provide insight into mechanisms that may regulate the development of other malignancies arising within the context of inflammatory states.
Richard M Peek - One of the best experts on this subject based on the ideXlab platform.
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use of the noninvasive entero test in the detection of helicobacter pylori in children in an endemic area in colombia
Journal of Pediatric Gastroenterology and Nutrition, 2013Co-Authors: Richard Arboleda, Richard M Peek, Barbara G. Schneider, Robertino M. Mera, Luis Eduardo Bravo, Judith Romerogallo, Maria Clara Yepez, Cristina Campo, Pelayo CorreaAbstract:Gastric cancer is the fourth most commonly diagnosed cancer and second leading cause of cancer deaths worldwide, responsible for 738,000 deaths in 20081. In many parts of the world, such as the Andean regions of Latin America, this disease is the most common cause of cancer-related death. Identification of Helicobacter pylori (H. pylori) as a risk factor for gastric cancer2 has revealed a new set of challenges for reducing the mortality of the disease. As part of ongoing studies in the natural history of infection, a cohort of children was previously established in the Andean region of Colombia, where H. pylori has a high prevalence in untreated children3, and the proportion of infected children increased with age (53% for 2-year-olds and 87% for 9 year-old asymptomatic children4). Large-scale investigations of H. pylori in asymptomatic children in endemic areas have been limited due to the inability to obtain biopsies for ethical reasons. The Entero-test (HDC Corporation, San Jose, CA) has been validated as a non-invasive procedure to obtain H. pylori from gastric samples, with a variable diagnostic efficacy of culture and/or PCR ranging from 37–97%5, 6. However, these studies have been performed in adults, and none have included children in an endemic area. Previous studies have shown a difference in the virulence of strains in children depending on age and history of treatment. For example, some reports indicate that genotypes recovered from children are less virulent than those of adults7. The virulence-associated genes cagA and vacA play a role in the pathogenesis of H. pylori. The cagA gene, which encodes a 120 to 145 kDa protein, is a marker for the cag pathogenicity island (PAI) and is found in more than 50% of H. pylori strains8. The cagA gene, closely associated with the vacA s1 genotype, is considered an inducer of pro-inflammatory cytokines in the gastric mucosa and is a risk factor for disease9, 10. The vacA gene encodes an 88-kDa vacuolating cytotoxin (VacA) that forms pores in eukaryotic cell membranes11. Within the vacA gene, three regions of marked sequence diversity can be distinguished: the s region (encoding the signal peptide) is present as either an s1 or an s2 allele, the intermediate region is present as either i1 or i2, and the m-region (the middle region of the toxin) can be either m1 or m212–14. The mosaic combination of s and m region alleles determines the production of the vacuolating cytotoxin and is associated with the pathogenicity of the bacterium. VacA s1m1 strains have been associated with increased virulence and greater gastric epithelial damage and ulceration than s2m2 strains12, 15. Our aim was to validate the use of the Entero-test as a non-invasive test to identify the presence of H. pylori and evaluate the prevalence of H. pylori specific virulence genotypes in an endemic area.
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helicobacter pylori perturbs iron trafficking in the epithelium to grow on the cell surface
PLOS Pathogens, 2011Co-Authors: Shumin Tan, Richard M Peek, Jennifer M Noto, Judith Romerogallo, Manuel R AmievaAbstract:Helicobacter pylori (Hp) injects the CagA effector protein into host epithelial cells and induces growth factor-like signaling, perturbs cell-cell junctions, and alters host cell polarity. This enables Hp to grow as microcolonies adhered to the host cell surface even in conditions that do not support growth of free-swimming bacteria. We hypothesized that CagA alters host cell physiology to allow Hp to obtain specific nutrients from or across the epithelial barrier. Using a polarized epithelium model system, we find that isogenic ΔcagA mutants are defective in cell surface microcolony formation, but exogenous addition of iron to the apical medium partially rescues this defect, suggesting that one of CagA's effects on host cells is to facilitate iron acquisition from the host. Hp adhered to the apical epithelial surface increase basolateral uptake of transferrin and induce its transcytosis in a CagA-dependent manner. Both CagA and VacA contribute to the perturbation of transferrin recycling, since VacA is involved in apical mislocalization of the transferrin receptor to sites of bacterial attachment. To determine if the transferrin recycling pathway is involved in Hp colonization of the cell surface, we silenced transferrin receptor expression during infection. This resulted in a reduced ability of Hp to colonize the polarized epithelium. To test whether CagA is important in promoting iron acquisition in vivo, we compared colonization of Hp in iron-replete vs. iron-deficient Mongolian gerbils. While wild type Hp and ΔcagA mutants colonized iron-replete gerbils at similar levels, ΔcagA mutants are markedly impaired in colonizing iron-deficient gerbils. Our study indicates that CagA and VacA act in concert to usurp the polarized process of host cell iron uptake, allowing Hp to use the cell surface as a replicative niche.
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helicobacter pylori dysregulation of gastric epithelial tight junctions by urease mediated myosin ii activation
Gastroenterology, 2009Co-Authors: Lydia E Wroblewski, Dawn A Israel, Le Shen, Seth R Ogden, Judith Romero Gallo, Lynne A Lapierre, Jerrold R Turner, Richard M PeekAbstract:Background & Aims Helicobacter pylori -induced gastritis predisposes to the development of gastric cancer. Increased epithelial tight junction permeability and alterations in apical-junctional complexes are also associated with an increased risk of carcinogenesis. Phosphorylation of myosin regulatory light chain (MLC) by MLC kinase (MLCK) regulates tight junction function. We determined whether MLCK was activated by H pylori and defined the mechanisms through which such activation dysregulates gastric epithelial barrier function. Methods MKN28 gastric epithelial cells were cocultured with the H pylori cag + strain 60190 or cagA − , cagE − , ureB − , or vacA − mutants. MLC phosphorylation and barrier integrity were determined by immunoblot analysis and transepithelial electrical resistance measurements, respectively. Localization of the tight junction protein occludin was determined by immunocytochemistry in MKN28 cells and INS-GAS mice. Results H pylori induced a progressive loss of barrier function that was attenuated by inactivation of ureB , but not cagA, cagE , or vacA . Reductions in transepithelial electrical resistance were also dependent on functional urease activity. H pylori increased MLC phosphorylation in epithelial monolayers; this was significantly decreased by inhibition of MLCK or Rho kinase or by loss of UreB. H pylori infection of either cultured monolayers or hypergastrinemic INS-GAS mice induced occludin endocytosis, reflecting cytoskeletally mediated disruption of tight junctions. Conclusions H pylori increases MLC phosphorylation, occludin internalization and barrier dysfunction in gastric epithelial cells. This process requires functional urease activity and is independent of the cag pathogenicity island or VacA. These data provide new insights into the mechanisms by which H pylori disrupts gastric barrier function.
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regulation of gastric carcinogenesis by helicobacter pylori virulence factors
Cancer Research, 2008Co-Authors: Aime T Franco, Yoshio Yamaoka, Elizabeth Johnston, Uma Krishna, Dawn A Israel, Toni A Nagy, Lydia E Wroblewski, Maria Blanca Piazuelo, Pelayo Correa, Richard M PeekAbstract:Helicobacter pylori is the strongest known risk factor for gastric adenocarcinoma, and strains that possess the cag secretion system, which translocates the bacterial effector CagA into host cells, augment cancer risk. H. pylori strains that express the vacuolating cytotoxin or the outer membrane protein OipA are similarly associated with severe pathologic outcomes. We previously reported that an in vivo adapted H. pylori strain, 7.13, induces gastric adenocarcinoma in rodent models of gastritis. In the current study, we used carcinogenic strain 7.13 as a prototype to define the role of virulence constituents in H. pylori-mediated carcinogenesis. Mongolian gerbils were infected with wild-type strain 7.13 or cagA(-), vacA(-), or oipA(-) mutants for 12 to 52 weeks. All infected gerbils developed gastritis; however, inflammation was significantly attenuated in animals infected with the cagA(-) but not the vacA(-) or oipA(-) strains. Gastric dysplasia and cancer developed in >50% of gerbils infected with either the wild-type or vacA(-) strain but in none of the animals infected with the cagA(-) strain. Inactivation of oipA decreased beta-catenin nuclear localization in vitro and reduced the incidence of cancer in gerbils. OipA expression was detected significantly more frequently among H. pylori strains isolated from human subjects with gastric cancer precursor lesions versus persons with gastritis alone. These results indicate that loss of CagA prevents the development of cancer in this model. Inactivation of oipA attenuates beta-catenin nuclear translocation and also decreases the incidence of carcinoma. In addition to defining factors that mediate H. pylori-induced cancer, these results provide insight into mechanisms that may regulate the development of other malignancies arising within the context of inflammatory states.
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helicobacter pylori strain selective induction of matrix metalloproteinase 7 in vitro and within gastric mucosa
Gastroenterology, 2003Co-Authors: Howard C Crawford, Uma Krishna, Dawn A Israel, Lynn M Matrisian, Kay M Washington, Richard M PeekAbstract:Abstract Background & Aims: Helicobacter pylori strains that possess the cag pathogenicity island ( cag + ) augment the risk for distal gastric cancer. Matrix metalloproteinase (MMP)-7, an epithelial cell-derived MMP that is induced by bacterial contact, is overexpressed within human gastric adenocarcinoma specimens and enhances tumor formation in rodents. We determined whether H. pylori alters MMP-7 expression and investigated the molecular pathways required for these events. Methods: MMP-7 was detected in human gastric mucosa by immunohistochemistry and in H. pylori /AGS gastric epithelial cell coculture supernatants by Western analysis. AGS cells were cocultured with wild-type H. pylori , or isogenic cagA − , cagE − , or vacA − mutants, in the absence or presence of inhibitors of nuclear factor κB activation, p38, or extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase. Results: H. pylori cag + strains increased MMP-7 expression in AGS cells 5–7-fold, whereas cag − isolates had no effect. Inactivation of cagE , but not cagA or vacA , completely attenuated induction of MMP-7, and inhibition of ERK 1/2 decreased MMP-7 production. In vivo, MMP-7 was expressed in gastric epithelial cells in specimens from 80% of cag + -colonized persons but in none of the cag − or uninfected subjects. Conclusions: H. pylori cag + strains enhance levels of MMP-7 within inflamed mucosa. In vitro, cag + isolates selectively induce MMP-7, and this is dependent on activation of ERK 1/2 by specific components within the cag island. Differential induction of MMP-7 by H. pylori cag + isolates may explain in part the augmentation in gastric cancer risk associated with these strains.
Boris Hespeels - One of the best experts on this subject based on the ideXlab platform.
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gateway to genetic exchange dna double strand breaks in the bdelloid rotifer adineta Vaga submitted to desiccation
Journal of Evolutionary Biology, 2014Co-Authors: Boris Hespeels, M Knapen, D Hanotmambres, Annecatherine Heuskin, F Pineux, Stephane Lucas, Romain Koszul, Karine Van DoninckAbstract:: The bdelloid rotifer lineage Adineta Vaga inhabits temporary habitats subjected to frequent episodes of drought. The recently published draft sequence of the genome of A. Vaga revealed a peculiar genomic structure incompatible with meiosis and suggesting that DNA damage induced by desiccation may have reshaped the genomic structure of these organisms. However, the causative link between DNA damage and desiccation has never been proven to date in rotifers. To test for the hypothesis that desiccation induces DNA double-strand breaks (DSBs), we developed a protocol allowing a high survival rate of desiccated A. Vaga. Using pulsed-field gel electrophoresis to monitor genomic integrity, we followed the occurrence of DSBs in dried bdelloids and observed an accumulation of these breaks with time spent in dehydrated state. These DSBs are gradually repaired upon rehydration. Even when the genome was entirely shattered into small DNA fragments by proton radiation, A. Vaga individuals were able to efficiently recover from desiccation and repair a large amount of DSBs. Interestingly, when investigating the influence of UV-A and UV-B exposure on the genomic integrity of desiccated bdelloids, we observed that these natural radiations also caused important DNA DSBs, suggesting that the genome is not protected during the desiccated stage but that the repair mechanisms are extremely efficient in these intriguing organisms.
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gateway to genetic exchange dna double strand breaks in the bdelloid rotifer adineta Vaga submitted to desiccation
Journal of Evolutionary Biology, 2014Co-Authors: Boris Hespeels, M Knapen, D Hanotmambres, Annecatherine Heuskin, F Pineux, Stephane Lucas, Romain Koszul, Karine Van DoninckAbstract:: The bdelloid rotifer lineage Adineta Vaga inhabits temporary habitats subjected to frequent episodes of drought. The recently published draft sequence of the genome of A. Vaga revealed a peculiar genomic structure incompatible with meiosis and suggesting that DNA damage induced by desiccation may have reshaped the genomic structure of these organisms. However, the causative link between DNA damage and desiccation has never been proven to date in rotifers. To test for the hypothesis that desiccation induces DNA double-strand breaks (DSBs), we developed a protocol allowing a high survival rate of desiccated A. Vaga. Using pulsed-field gel electrophoresis to monitor genomic integrity, we followed the occurrence of DSBs in dried bdelloids and observed an accumulation of these breaks with time spent in dehydrated state. These DSBs are gradually repaired upon rehydration. Even when the genome was entirely shattered into small DNA fragments by proton radiation, A. Vaga individuals were able to efficiently recover from desiccation and repair a large amount of DSBs. Interestingly, when investigating the influence of UV-A and UV-B exposure on the genomic integrity of desiccated bdelloids, we observed that these natural radiations also caused important DNA DSBs, suggesting that the genome is not protected during the desiccated stage but that the repair mechanisms are extremely efficient in these intriguing organisms.
