DNMT1 mutant ants develop normally, but have disrupted oogenesis and decreased survival
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ABSTRACT:
PROVIDER: PRJNA755311 | ENA |
REPOSITORIES: ENA
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Project description:While DNA methylation is an important gene regulatory mechanism in mammals (Razin and Riggs 1980; Moore, Le, and Fan 2013), its function in arthropods remains poorly understood. Studies in eusocial insects have argued for its role in caste development by regulating gene expression and splicing (Elango et al. 2009; Lyko et al. 2010; Bonasio et al. 2012; Flores et al. 2012; Foret et al. 2012; Li-Byarlay et al. 2013; Marshall, Lonsdale, and Mallon 2019; Shi et al. 2013)(Alvarado et al. 2015; Kucharski et al. 2008). However, such findings are not always consistent across studies, and have therefore remained controversial (Arsenault, Hunt, and Rehan 2018; Cardoso-Junior et al. 2021; Harris et al. 2019; Herb et al. 2012; Libbrecht et al. 2016; Oldroyd and Yagound 2021b; Patalano et al. 2015). Here we use CRISPR/Cas9 to mutate the maintenance DNA methyltransferase DNMT1 in the clonal raider ant, Ooceraea biroi. Mutants have greatly reduced DNA methylation but no obvious developmental phenotypes, demonstrating that, unlike mammals (Brown and Robertson 2007; En Li, Bestor, and Jaenisch 1992; Jackson-Grusby et al. 2001; Panning and Jaenisch 1996), ants can undergo normal development without DNMT1 or DNA methylation. Additionally, we find no evidence of DNA methylation regulating caste development. However, mutants are sterile, while in wildtypes, DNMT1 is localized to the ovaries and maternally provisioned into nascent oocytes. This supports the idea that DNMT1 plays a crucial but unknown role in the insect germline (Amukamara et al. 2020; Arsala et al. 2021; Bewick et al. 2019; Schulz et al. 2018; Ventós-Alfonso et al. 2020; Washington et al. 2020).
2023-03-23 | GSE182212 | GEO
Project description:Although DNA methylation is an important gene regulatory mechanism in mammals, its function in arthropods remains poorly understood. Studies in eusocial insects have argued for its role in caste development by regulating gene expression and splicing. However, such findings are not always consistent across studies, and have therefore remained controversial. Here we use CRISPR/Cas9 to mutate the maintenance DNA methyltransferase DNMT1 in the clonal raider ant, Ooceraea biroi. Mutants have greatly reduced DNA methylation, but no obvious developmental phenotypes, demonstrating that, unlike mammals, ants can undergo normal development without DNMT1 or DNA methylation. Additionally, we find no evidence of DNA methylation regulating caste development. However, mutants are sterile, whereas in wild-type ants, DNMT1 is localized to the ovaries and maternally provisioned into nascent oocytes. This supports the idea that DNMT1 plays a crucial but unknown role in the insect germline.
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Project description:Deltex1, Deltex2, and Deltex4 form a family of related proteins that are the mammalian homologues of Drosophila Deltex, a known regulator of Notch signals. Deltex1 is highly induced by Notch signaling in thymocytes, and overexpression of Deltex1 in T-cell progenitors can block Notch signals, suggesting that Deltex1 may play an important role in regulating Notch signals during T-cell development. A recent report found that T cells develop normally in mice carrying a targeted deletion in the Deltex1 gene (S. Storck, F. Delbos, N. Stadler, C. Thirion-Delalande, F. Bernex, C. Verthuy, P. Ferrier, J. C. Weill, and C. A. Reynaud, Mol. Cell. Biol. 25: 1437-1445, 2005), suggesting that other Deltex homologues may compensate in Deltex1-deficient T cells. We generated mice that lack expression of both Deltex1 and Deltex2 by gene targeting and further reduced expression of Deltex4 in Deltex1/Deltex2 double-deficient T-cell progenitors using RNA interference. Using a sensitive in vitro assay, we found that Notch signaling is more potent in cells expressing lower levels of Deltex proteins. Nevertheless, we were unable to detect any significant defects in thymocyte maturation in Deltex1/Deltex2 double-knockout mice. Together these data suggest that Deltex can act as a negative regulator of Notch signals in T cells but that endogenous levels of Deltex1 and Deltex2 are not important for regulating Notch signals during thymocyte development.
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