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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.
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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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Journal ArticleDOI

Mechanisms generating cancer genome complexity from a single cell division error

TL;DR: This work recreated essential steps of the BFB cycle in a defined system, enabling mechanistic studies and determination of the immediate and long-term genomic consequences of bridge formation, suggesting a unifying model for how cancer-associated defects in nuclear architecture is handled.
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Microcell-mediated transfer of murine chromosomes into mouse, Chinese hamster, and human somatic cells.

TL;DR: The production and characterization of proliferating hybrid cell populations generated by fusion of murine microcells with intact mouse, Chinese hamster, and human recipient cells are described.
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Autophagic cell death restricts chromosomal instability during replicative crisis.

TL;DR: It is shown that macroautophagy has a dominant role in the death of fibroblasts and epithelial cells during crisis and that loss of autophagy function is required for the initiation of cancer.
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The Cytoplasmic DNA Sensor cGAS Promotes Mitotic Cell Death

TL;DR: It is proposed that slow accumulation of phosphorylated IRF3, normally not sufficient for inducing inflammation, can trigger transcription-independent induction of apoptosis upon mitotic aberrations.
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Nuclear envelope assembly defects link mitotic errors to chromothripsis

TL;DR: It is shown that spindle microtubules block assembly of NPCs and other non-core nuclear envelope proteins on lagging chromosomes, causing an irreversible defect in nuclear envelope assembly, which leads to spontaneous envelope disruption of micronuclei and subsequent genome instability.
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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.