Cell
ArticleV(D)J recombination: Broken DNA molecules with covalently sealed (hairpin) coding ends in scid mouse thymocytes
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2020, iScienceCitation Excerpt :Although we could detect robust and efficient conversion of fully and properly recombined SJ + CJ products of the pMG-INV recombination substrate in induced Setd2-deficient v-Abl cells, we could also detect, with combined loss of Atm kinase activity, an aberrant SJ + CE recombination product. This raises the possibility of a CE-specific hairpin opening/repair defect, which would certainly require further study as CEs are thought be efficiently processed and repaired at a much higher rate than SEs and CE-only defects have not previously been reported (Ramsden and Gellert, 1995; Schlissel et al., 1993; Roth, et al., 1992; Canela et al., 2016; Meek et al., 2016). Paradoxically, whereas the end-ligation defect of Setd2/H3K36me3 loss, as determined by the assessment of a recombination substrate in transformed v-Abl cells, may appear subtle, in mice, its loss severely arrests normal B/T lymphocyte development, similar to what is observed in mice with loss of C-NHEJ factors (Alt et al., 2013; Kumar et al., 2014) and in contrast to loss of factors involved in end-ligation, such as Atm, Xlf, Paxx, or Mri individually (Bredemeyer et al., 2006; Kumar et al., 2016; Hung et al., 2018; Li et al., 2008; Lescale et al., 2016; Zha et al., 2011).
Atypical ploidy cycles, Spo11, and the evolution of meiosis
2016, Seminars in Cell and Developmental Biology