Unrepaired DNA damage facilitates elimination of uniparental chromosomes in interspecific hybrid cells

Wang, Zheng; Yin, Hong; Lv, Lei; Feng, Yingying; Chen, Shaopeng; Liang, Junting; Huang, Yun; Jiang, Xiaohua; Jiang, Hanwei; Bukhari, Ihtisham; Wu, Lijun; Cooke, Howard J.; Shi, Qinghua

doi:10.4161/cc.28296

Cited by 12 publications

(10 citation statements)

References 66 publications

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“…Parent‐specific haploidization can thus attribute to early loss of the wild‐type LIG4 allele located on inducer chromosomes, and formation of diploids and aneuploids results from LIG4‐dependent chromosome rescue. In mammalian systems, the frequency of uniparental chromosome elimination can be increased by unrepaired DNA damage (Wang et al ., ). Overall, DNA repair mutants may be used to increase haploid induction rates in the CENH3‐mediated genome elimination system (Britt and Kuppu, ).…”

Section: Haploidization Via Chromosome Eliminationmentioning

confidence: 97%

Novel technologies in doubled haploid line development

Ren

Trampe

et al. 2017

Plant Biotechnology Journal

121

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Summaryhaploid inducer line can be transferred (DH) technology can not only shorten the breeding process but also increase genetic gain. Haploid induction and subsequent genome doubling are the two main steps required for DH technology. Haploids have been generated through the culture of immature male and female gametophytes, and through inter‐ and intraspecific via chromosome elimination. Here, we focus on haploidization via chromosome elimination, especially the recent advances in centromere‐mediated haploidization. Once haploids have been induced, genome doubling is needed to produce DH lines. This study has proposed a new strategy to improve haploid genome doubling by combing haploids and minichromosome technology. With the progress in haploid induction and genome doubling methods, DH technology can facilitate reverse breeding, cytoplasmic male sterile (CMS) line production, gene stacking and a variety of other genetic analysis.

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Section: Haploidization Via Chromosome Eliminationmentioning

confidence: 97%

Novel technologies in doubled haploid line development

Ren

Trampe

et al. 2017

Plant Biotechnology Journal

121

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“…63 Cells grown on coverslips were permeabilized with PBS containing 0.25% Triton X-100 for 5 min. The primary antibodies included rabbit anti-53BP1 (NB100-305, 1:200; Novus Biologicals), Mouse anti-g-H2AX (05-636,1:250; Millipore), rabbit anti-Rad51 (H-92, 1:200; Santa Cruz), goat antiBrca1 (M20, 1:200; Santa Cruz) and human auto-antibody against centromere antibody (HCT-0100, 1:100; Immunovision).…”

Section: Immunofluorescence Stainingmentioning

confidence: 99%

miR-214-mediated downregulation of RNF8 induces chromosomal instability in ovarian cancer cells

et al. 2014

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Defective DNA damage response (DDR) is frequently associated with carcinogenesis. Abrogation of DDR leads to chromosomal instability, a most common characteristic of tumors. However, the molecular mechanisms underlying regulation of DDR are still elusive. The ubiquitin ligase RNF8 mediates the ubiquitination of gH2AX and recruits 53BP1 and BRCA1 to DNA damage sites which promotes DDR and inhibits chromosomal instability. Though RNF8 is a key player involved in DDR, regulation of its expression is still poorly understood. Here, we show that miR-214 could abrogate DDR by repressing RNF8 expression through direct binding to 3 0 -untranslated region (3 0 UTR) of RNF8 mRNA in human ovarian cancer cells. Antagonizing miR-214 by expressing its inhibitors in A2780 cells significantly increased RNF8 expression and thus promoted DNA damage repair. Consistent with the role of miR-214 in regulating RNF8 expression, the impaired DNA repair induced by miR-214 overexpression can be rescued by overexpressing RNF8 mRNA lacking the 3 0 UTR. Together, our results indicate that down-regulation of RNF8 mediated by miR-214 impedes DNA damage response to induce chromosomal instability in ovarian cancers, which may facilitate the understanding of mechanisms underlying chromosomal instability.

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“…Certain models and experiments show that increase in mutation rates may accelerate adaptation (Taddei et al 1997;Schaaff et al 2002;Labat et al 2005;Le Bars et al 2014;Bui et al 2015;Couce et al 2017) . Genomic instability includes higher rate of DNA damage (Wang et al 2014;Herbst et al 2017) , chromosomal rearrangements (Baack & Rieseberg 2007;Mwathi et al 2019) , gene and chromosome copy number variation (Morales & Dujon 2012;Dion-Côté & Barbash 2017) and the multiplication of repetitive and transposable elements (Fontdevila 2005;Guerreiro 2014) . These changes often lead to aneuploidy, which has also been shown to be a mechanism of adaptation in stressful conditions (Mulla et al 2014;Sunshine et al 2015) and hybrids may be particularly prone to producing aneuploid progeny (Gilchrist & Stelkens 2019) .…”

Section: Introductionmentioning

confidence: 99%

Interspecific Hybrids Show a Reduced Adaptive Potential Under DNA Damaging Conditions

Bautista

Marsit

Landry

2020

Preprint

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AbstractHybridization may increase the probability of adaptation to extreme stresses. This advantage could be caused by an increased genome plasticity in hybrids, which could accelerate the search for adaptive mutations. High ultraviolet (UV) radiation is a particular challenge in terms of adaptation because it affects the viability of organisms by directly damaging DNA, while also challenging future generations by increasing mutation rate. Here we test if hybridization accelerates adaptive evolution in response to DNA damage, using yeast as a model. We exposed 180 populations of hybrids between species (Saccharomyces cerevisiae and Saccharomyces paradoxus) and their parental strains to UV mimetic and control conditions for approximately 100 generations. Although we found that adaptation occurs in both hybrids and parents, hybrids achieved a lower rate of adaptation, contrary to our expectations. Adaptation to DNA damage conditions comes with a large and similar cost for parents and hybrids, suggesting that this cost is not responsible for the lower adaptability of hybrids. We suggest that the lower adaptive potential of hybrids in this condition may result from the interaction between DNA damage and the inherent genetic instability of hybrids.

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Unrepaired DNA damage facilitates elimination of uniparental chromosomes in interspecific hybrid cells

Cited by 12 publications

References 66 publications

Novel technologies in doubled haploid line development

Novel technologies in doubled haploid line development

miR-214-mediated downregulation of RNF8 induces chromosomal instability in ovarian cancer cells

Interspecific Hybrids Show a Reduced Adaptive Potential Under DNA Damaging Conditions

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