A C. elegans homolog of the Cockayne syndrome complementation group A gene |
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| Institution: | 1. Institute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne, 50931 Cologne, Germany;2. Cologne Excellence Cluster for Cellular Stress Responses in Ageing-Associated Diseases (CECAD) Research Center and Systems Biology of Ageing Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany;3. Institute for Genetics, University of Cologne, Zülpicher Str. 47a, 50674 Cologne, Germany;3. North Carolina Oral Health Institute, School of Dentistry, University of North Carolina, Chapel Hill, North Carolina 27599;4. Nippi Research Institute of Biomatrix, Ibaraki 302-0017, Japan;5. Department of Thoracic/Head and Neck Medical Oncology, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030;12. Division of Bio-Prosthodontics, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8514, Japan;1. National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN), 7-6-8 Saito-Asagi, Ibaraki, Osaka, 567-0085, Japan;2. Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka, Suita, Osaka, 565-0871, Japan;3. Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamadaoka, Suita, Osaka, 565-0871, Japan;3. Institute of Translational Pharmacology, Consiglio Nazionale delle Ricerche (CNR), 00133 Rome, Italy;4. Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy;1. Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako, Saitama, Japan;2. Laboratory for Molecular Brain Science, Department of Life Science and Medical Bioscience, Waseda University, Shinjuku, Tokyo, Japan;3. Department of Functional Anatomy and Neuroscience, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan;4. Department of Neurocognitive Science, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, Japan |
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| Abstract: | Cockayne syndrome (CS) is a debilitating and complex disorder that results from inherited mutations in the CS complementation genes A and B, CSA and CSB. The links between the molecular functions of the CS genes and the complex pathophysiology of CS are as of yet poorly understood and are the subject of intense debate. While mouse models reflect the complexity of CS, studies on simpler genetic models might shed new light on the consequences of CS mutations. Here we describe a functional homolog of the human CSA gene in Caenorhabditis elegans. Similar to its human counterpart, mutations in the nematode csa-1 gene lead to developmental growth defects as a consequence of DNA lesions. |
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