Abstract：
:Nuclear β-dystroglycan (β-DG) is involved in the maintenance of nuclear architecture and function. Nonetheless, its relevance in defined nuclear processes remains to be determined. In this study we generated a C2C12 cell-based DG-null model using CRISPR-Cas9 technology to provide insights into the role of β-DG on nuclear processes. Since DG-null cells exhibited decreased levels of lamin B1, we aimed to elucidate the contribution of DG to senescence, owing to the central role of lamin B1 in this pathway. Remarkably, the lack of DG enables C2C12 cells to acquire senescent features, including cell-cycle arrest, increased senescence-associated-β-galactosidase activity, heterochromatin loss, aberrant nuclear morphology and nucleolar disruption. We demonstrated that genomic instability is one driving cause of the senescent phenotype in DG-null cells via the activation of a DNA-damage response associated with mitotic failure, as shown by the presence of multipolar mitotic spindles, which in turn induced the formation of micronuclei and γH2AX foci (DNA-damage marker), telomere shortening and p53/p21 upregulation. Altogether, these events might ultimately lead to premature senescence, impeding the replication of the damaged genome. In summary, we present evidence supporting a role for DG in protecting against senescence, through the maintenance of proper lamin B1 expression/localization and proper mitotic spindle organization.
journal_name
Int J Mol Scijournal_title
International journal of molecular sciencesauthors
Jimenez-Gutierrez GE,Mondragon-Gonzalez R,Soto-Ponce LA,Gómez-Monsiváis WL,García-Aguirre I,Pacheco-Rivera RA,Suárez-Sánchez R,Brancaccio A,Magaña JJ,C R Perlingeiro R,Cisneros Bdoi
10.3390/ijms21144961subject
Has Abstractpub_date
2020-07-14 00:00:00issue
14issn
1422-0067pii
ijms21144961journal_volume
21pub_type
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