Generation and Characterization of the Anp32e-Deficient Mouse

Reilly, Patrick T.; Afzal, Samia; Wakeham, Andrew; Haight, Jillian; You-Ten, Annick; Zaugg, Kathrin; Dembowy, Joanna; Young, A.C.; Mak, Tak W.

doi:10.1371/journal.pone.0013597

Cited by 25 publications

(29 citation statements)

References 41 publications

(69 reference statements)

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“…The data we have presented here, as well as in a previous publication (35), demonstrate that the Anp32 genes are not likely to be broadly involved in apoptosis. Furthermore, no ANP32-deficient cells have yet shown proliferation defects, implying that ANP32-mediated inhibition of cell cycle control phosphatases, such as PP2A, may be redundant or have a limited impact on cell proliferation.…”

Section: Discussionsupporting

confidence: 63%

“…We have previously reported that neither the ANP32A-deficient nor the ANP32E-deficient mouse has any obvious abnormal phenotype (35). To determine whether deficiency for another Anp32 family member might expose the cause of the viability defect of our Anp32b −/− mice, we generated Anp32b +/− ;Anp32a +/− and Anp32b +/− ;Anp32e +/− double-mutant strains and intercrossed them.…”

Section: Resultsmentioning

confidence: 99%

“…Sequences directing the expression of diphtheria toxin A in mouse ES cells were cloned into pBluescript (pgk-neo) to give the plasmid pBSneoDTA (35). Regions of the Anp32b gene adjacent to the targeted exons were cloned by high-fidelity PCR.…”

Section: Methodsmentioning

confidence: 99%

“…Apoptosis assays were performed as described previously (35,44). Briefly, cells were exposed to apoptotic stimuli as detailed in Fig.…”

Section: Methodsmentioning

confidence: 99%

“…Reported loss-of-function mutants for ANP32 family members include two independently targeted ANP32A-deficient mice (34,35), an ANP32E-deficient mouse (35), and a presumptive null mutant of mapmodulin in Drosophila (36). All of these mutants were viable and fertile with no obvious abnormalities.…”

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confidence: 99%

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Acidic nuclear phosphoprotein 32kDa (ANP32)B-deficient mouse reveals a hierarchy of ANP32 importance in mammalian development

Reilly

Afzal²,

Gorrini³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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The highly conserved ANP32 proteins are proposed to function in a broad array of physiological activities through molecular mechanisms as diverse as phosphatase inhibition, chromatin regulation, caspase activation, and intracellular transport. On the basis of previous analyses of mice bearing targeted mutations of Anp32a or Anp32e, there has been speculation that all ANP32 proteins play redundant roles and are dispensable for normal development. However, more recent work has suggested that ANP32B may in fact have functions that are not shared by other ANP32 family members. Here we report that ANP32B expression is associated with a poor prognosis in human breast cancer, consistent with the increased levels of Anp32b mRNA present in proliferating wild-type (WT) murine embryonic fibroblasts and stimulated WT B and T lymphocytes. Moreover, we show that, contrary to previous assumptions, Anp32b is very important for murine embryogenesis. In a mixed genetic background, ANP32B-deficient mice displayed a partially penetrant perinatal lethality that became fully penetrant in a pure C57BL/6 background. Surviving ANP32B-deficient mice showed reduced viability due to variable defects in various organ systems. Study of compound mutants lacking ANP32A, ANP32B, and/or ANP32E revealed previously hidden roles for ANP32A in mouse development that became apparent only in the complete absence of ANP32B. Our data demonstrate a hierarchy of importance for the mammalian Anp32 genes, with Anp32b being the most critical for normal development.cell growth | mouse embryogenesis | premature aging

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Section: Discussionsupporting

confidence: 63%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…Apoptosis assays were performed as described previously (35,44). Briefly, cells were exposed to apoptotic stimuli as detailed in Fig.…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Acidic nuclear phosphoprotein 32kDa (ANP32)B-deficient mouse reveals a hierarchy of ANP32 importance in mammalian development

Reilly

Afzal²,

Gorrini³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Hierarchical Accumulation of Histone Variant H2A.Z Regulates Transcriptional States and Histone Modifications in Early Mammalian Embryos

et al. 2022

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Early embryos undergo extensive epigenetic reprogramming to achieve gamete‐to‐embryo transition, which involves the loading and removal of histone variant H2A.Z on chromatin. However, how does H2A.Z regulate gene expression and histone modifications during preimplantation development remains unrevealed. Here, by using ultra‐low‐input native chromatin immunoprecipitation and sequencing, the genome‐wide distribution of H2A.Z is delineated in mouse oocytes and early embryos. These landscapes indicate that paternal H2A.Z is removed upon fertilization, followed by unbiased accumulation on parental genomes during zygotic genome activation (ZGA). Remarkably, H2A.Z exhibits hierarchical accumulation as different peak types at promoters: promoters with double H2A.Z peaks are colocalized with H3K4me3 and indicate transcriptional activation; promoters with a single H2A.Z peak are more likely to occupy bivalent marks (H3K4me3+H3K27me3) and indicate development gene suppression; promoters with no H2A.Z accumulation exhibit persisting gene silencing in early embryos. Moreover, H2A.Z depletion changes the enrichment of histone modifications and RNA polymerase II binding at promoters, resulting in abnormal gene expression and developmental arrest during lineage commitment. Furthermore, similar transcription and accumulation patterns between mouse and porcine embryos indicate that a dual role of H2A.Z in regulating the epigenome required for proper gene expression is conserved during mammalian preimplantation development.

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Cracking the ANP32 whips: Important functions, unequal requirement, and hints at disease implications

Reilly

Hamiche

et al. 2014

BioEssays

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The acidic (leucine-rich) nuclear phosphoprotein 32 kDa (ANP32) family is composed of small, evolutionarily conserved proteins characterized by an N-terminal leucine-rich repeat domain and a C-terminal low-complexity acidic region. The mammalian family members (ANP32A, ANP32B, and ANP32E) are ascribed physiologically diverse functions including chromatin modification and remodelling, apoptotic caspase modulation, protein phosphatase inhibition, as well as regulation of intracellular transport. In addition to reviewing the widespread literature on the topic, we present a concept of the ANP32s as having a whip-like structure. We also present hypotheses that ANP32C and other intronless sequences should not currently be considered bona fide family members, that their disparate necessity in development may be due to compensatory mechanisms, that their contrasting roles in cancer are likely context-dependent, along with an underlying hypothesis that ANP32s represent an important node of physiological regulation by virtue of their diverse biochemical activities.

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Generation and Characterization of the Anp32e-Deficient Mouse

Cited by 25 publications

References 41 publications

Acidic nuclear phosphoprotein 32kDa (ANP32)B-deficient mouse reveals a hierarchy of ANP32 importance in mammalian development

Acidic nuclear phosphoprotein 32kDa (ANP32)B-deficient mouse reveals a hierarchy of ANP32 importance in mammalian development

Hierarchical Accumulation of Histone Variant H2A.Z Regulates Transcriptional States and Histone Modifications in Early Mammalian Embryos

Cracking the ANP32 whips: Important functions, unequal requirement, and hints at disease implications

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