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Causes and consequences of micronuclei.

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TLDR
In this paper, the authors discuss how micronuclei are generated, what the consequences are, and what cellular mechanisms can be applied to protect against micronuclearation, with a focus on the effects of DNA degradation.
About
This article is published in Current Opinion in Cell Biology.The article was published on 2021-06-01. It has received 60 citations till now. The article focuses on the topics: Chromothripsis & DNA repair.

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Citations
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DNA damage and repair in age-related inflammation

TL;DR: In this article , the authors discuss the mechanisms by which DNA damage induces inflammation, such as through activation of the cGAS-STING axis and NF-κB activation by ATM.
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Current Methods and Pipelines for Image-Based Quantitation of Nuclear Shape and Nuclear Envelope Abnormalities

TL;DR: An overview of several nuclear abnormalities, including micronuclei, nuclear envelope invaginations, blebs and ruptures, and current methods used for image-based quantification of these abnormalities are reviewed, and several parameters that can be used to quantify nuclear shape are discussed.
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Telomeric 8-oxo-guanine drives rapid premature senescence in the absence of telomere shortening

TL;DR: In this paper , the authors proposed that oxidative stress promotes rapid senescence by producing oxidative base lesions that drive replication-dependent telomere fragility and dysfunction in the absence of shortening and shelterin loss.
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Principles and functions of pericentromeric satellite DNA clustering into chromocenters.

TL;DR: In this article , a review of the literature on pericentromeric satellite DNA and its organization and functions across eukaryotic species is presented, focusing on chromocenters.
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Spontaneous activity of the mitochondrial apoptosis pathway drives chromosomal defects, the appearance of micronuclei and cancer metastasis through the Caspase-Activated DNAse

TL;DR: In this article , the authors tested whether spontaneously appearing micronuclei in cancer cells are linked to sub-lethal apoptotic signals and found that low-level activity in the mitochondrial apoptosis apparatus operates through CAD-dependent gene induction and STING-activation and has substantial impact on metastasis in cancer patients.
References
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Bloom syndrome protein restrains innate immune sensing of micronuclei by cgas

TL;DR: It is shown that BLM-deficient fibroblasts show constitutive up-regulation of inflammatory interferon-stimulated gene (ISG) expression, which is mediated by the cGAS–STING–IRF3 cytosolic DNA–sensing pathway, thus connecting DNA damage to cellular innate immune response, which may contribute to human pathogenesis.
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Mitotic chromosome alignment ensures mitotic fidelity by promoting interchromosomal compaction during anaphase.

TL;DR: These studies support a model in which the alignment of mitotic chromosomes promotes proper organization of chromosomes into a single nucleus and continued proliferation by ensuring that chromosomes segregate as a compact mass during anaphase.
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Chromosomes trapped in micronuclei are liable to segregation errors

TL;DR: Micronuclei, which are common in cancer cells, are prone to missegregation owing to kinetochore assembly defects, which represents a mechanism to delay the reincorporation of excess chromosome(s) and/or damaged DNA.
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STING-dependent paracriny shapes apoptotic priming of breast tumors in response to anti-mitotic treatment

TL;DR: It is shown that a proapoptotic secretory phenotype is induced by activation of cGAS/STING in cancer cells that are hit by antimitotic treatment, accumulate micronuclei and maintain mitochondrial integrity despite intrinsic apoptotic pressure.
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Micronuclei-based model system reveals functional consequences of chromothripsis in human cells

TL;DR: It is shown that the isolated micronuclei lack functional lamin B1 and become prone to envelope rupture, which leads to DNA damage and aberrant replication, and the proper assembly of nuclear envelope might be sensitive to membrane curvature.
Related Papers (5)
Trending Questions (1)
How to identify micronuclear dysfunction?

Micronuclear dysfunction can be identified by compromised integrity of the micronuclear envelope, delayed or disrupted DNA replication, inhibited DNA repair, and exposure of micronuclear DNA to the cytoplasm.