Spontaneous homologous recombination repair is decreased in the absence of ATR <i>in vivo</i>.

<p>Schematic representation of the <i>p^un</i> mutation (tandem duplication of exons 6–18) in which a HR-mediated event facilitates the deletion of one copy of the repeat resulting in the reversion of the mutant allele to a functional <i>p</i> gene. Reversion (HR) events are scored phenotypically by counting the numbers of single or groups of cells in the RPE with brown pigmentation in their cytoplasm. (<b>A</b>). Loss of one copy of <i>Atr</i> does not affect HR frequency (<i>i.e.</i> the number of <i>p^un</i> reversion events per RPE) (<b>Bi</b> and <b>ii</b>), whereas complete loss of ATR resulted in the significant decrease of HR frequency (<b>Bi</b> and <b>ii</b>). Within the outer clear region of <i>Atr^cond/−</i> normal eyes (<i>i.e.</i> no β-gal activity suggesting the presence of a single copy of <i>Atr</i>), the HR frequency was not different from <i>Trp1-Cre^tg/o</i> and <i>Atr^cond/+</i> in similar regions (<b>Biii</b>). Representative eye spot images from different genotypes in B. Pigmentation can be observed in the cytoplasm following a <i>p^un</i> reversion event in the RPE. Blue nuclei indicate nuclear-localized Cre activity (<b>C</b>). For (<b>B</b> and <b>C</b>) (s) <i>Atr^cond/−</i> small and (n) <i>Atr^cond/−</i> normal eyes; *<i>P<0.05</i> and ***<i>P<0.001</i>.