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Mutations in genes that ensure genome stability lead to human developmental syndromes. Mutations in Ataxia Telangiectasia and Rad3-related (\n                    <jats:italic>ATR<\/jats:italic>\n                    ) or in ATR-interacting protein (\n                    <jats:italic>ATRIP<\/jats:italic>\n                    ) lead to Seckel syndrome, which is characterized by developmental malformations and short life expectancy. While the roles of ATR in replicative stress response and chromosomal segregation are well established, it is unknown how ATRIP contributes to maintaining genomic stability in progenitor cells in vivo. Here, we generated the first mouse model to investigate ATRIP function. Conditional inactivation of\n                    <jats:italic>Atrip<\/jats:italic>\n                    in progenitor cells of the CNS and eye led to microcephaly, microphthalmia and postnatal lethality. To understand the mechanisms underlying these malformations, we used lens progenitor cells as a model and found that ATRIP loss promotes replicative stress and TP53-dependent cell death.\n                    <jats:italic>Trp53<\/jats:italic>\n                    inactivation in\n                    <jats:italic>Atrip<\/jats:italic>\n                    -deficient progenitor cells rescued apoptosis, but increased mitotic DNA damage and mitotic defects. Our findings demonstrate an essential role of ATRIP in preventing DNA damage accumulation during unchallenged replication.\n                  <\/jats:p>","DOI":"10.1038\/s41419-020-03090-9","type":"journal-article","created":{"date-parts":[[2020,10,27]],"date-time":"2020-10-27T23:02:58Z","timestamp":1603839778000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["ATRIP protects progenitor cells against DNA damage in vivo"],"prefix":"10.1038","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4085-7810","authenticated-orcid":false,"given":"Gabriel E.","family":"Matos-Rodrigues","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paulius","family":"Grigaravicius","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bernard S.","family":"Lopez","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas G.","family":"Hofmann","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8142-3878","authenticated-orcid":false,"given":"Pierre-Olivier","family":"Frappart","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8420-6991","authenticated-orcid":false,"given":"Rodrigo A. P.","family":"Martins","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2020,10,28]]},"reference":[{"key":"3090_CR1","doi-asserted-by":"publisher","unstructured":"O\u2019Driscoll, M. Diseases associated with defective responses to DNA damage. Cold Spring Harb. Perspect. Biol. 4, https:\/\/doi.org\/10.1101\/cshperspect.a012773 (2012).","DOI":"10.1101\/cshperspect.a012773"},{"key":"3090_CR2","doi-asserted-by":"crossref","first-page":"1071","DOI":"10.1038\/nature08467","volume":"461","author":"SP Jackson","year":"2009","unstructured":"Jackson, S. P. & Bartek, J. The DNA-damage response in human biology and disease. Nature 461, 1071\u20131078 (2009).","journal-title":"Nature"},{"key":"3090_CR3","doi-asserted-by":"crossref","first-page":"179","DOI":"10.1016\/j.molcel.2010.09.019","volume":"40","author":"A Ciccia","year":"2010","unstructured":"Ciccia, A. & Elledge, S. J. The DNA damage response: making it safe to play with knives. Mol. Cell 40, 179\u2013204 (2010).","journal-title":"Mol. Cell"},{"key":"3090_CR4","doi-asserted-by":"crossref","first-page":"1095","DOI":"10.1016\/j.celrep.2013.10.027","volume":"5","author":"JK Eykelenboom","year":"2013","unstructured":"Eykelenboom, J. K. et al. ATR activates the S-M checkpoint during unperturbed growth to ensure sufficient replication prior to mitotic onset. Cell Rep. 5, 1095\u20131107 (2013).","journal-title":"Cell Rep."},{"key":"3090_CR5","doi-asserted-by":"crossref","first-page":"806","DOI":"10.1126\/science.aap9346","volume":"361","author":"JC Saldivar","year":"2018","unstructured":"Saldivar, J. C. et al. An intrinsic S\/G2 checkpoint enforced by ATR. Science 361, 806\u2013810 (2018).","journal-title":"Science"},{"key":"3090_CR6","doi-asserted-by":"crossref","first-page":"616","DOI":"10.1038\/nrm2450","volume":"9","author":"KA Cimprich","year":"2008","unstructured":"Cimprich, K. A. & Cortez, D. ATR: an essential regulator of genome integrity. Nat. Rev. Mol. Cell Biol. 9, 616\u2013627 (2008).","journal-title":"Nat. Rev. Mol. Cell Biol."},{"key":"3090_CR7","doi-asserted-by":"crossref","first-page":"622","DOI":"10.1038\/nrm.2017.67","volume":"18","author":"JC Saldivar","year":"2017","unstructured":"Saldivar, J. C., Cortez, D. & Cimprich, K. A. The essential kinase ATR: ensuring faithful duplication of a challenging genome. Nat. Rev. Mol. Cell Biol. 18, 622\u2013636 (2017).","journal-title":"Nat. Rev. Mol. Cell Biol."},{"key":"3090_CR8","doi-asserted-by":"publisher","first-page":"1713","DOI":"10.1126\/science.1065521","volume":"294","author":"D Cortez","year":"2001","unstructured":"Cortez, D., Guntuku, S., Qin, J. & Elledge, S. J. ATR and ATRIP: partners in checkpoint signaling. 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