Fig. 4: Aggregation of MAVS is a feature of senescent cells and plays a role in SASP regulation. | Nature Communications

Fig. 4: Aggregation of MAVS is a feature of senescent cells and plays a role in SASP regulation.

From: Mitochondrial RNA cytosolic leakage drives the SASP

Fig. 4: Aggregation of MAVS is a feature of senescent cells and plays a role in SASP regulation.The alternative text for this image may have been generated using AI.

a Representative super-resolution Airyscan microscopy image of TOM20 (green) and MAVS (red) in proliferating and senescent (IR) MRC5 fibroblasts showing MAVS aggregation in senescent cells. Arrows indicate MAVS aggregates that are amplified on the right. Scale bar=10 μm. b The mean number of MAVS aggregates observed in proliferating and senescent MRC5 human fibroblasts. n = 5 independent experiments. Statistical significance was assessed by a two-sided Student’s unpaired t-test. p = 0.0001. Data are mean ± s.e.m. c Western blot showing successful small interfering RNA (siRNA) knockdown of MAVS in senescent MRC5 human fibroblasts. n = 3 independent experiments. d Column-clustered heatmap of SASP genes upregulated in senescent cells and significantly downregulated upon knockdown of MAVS. Color intensity represents the z-score. n = 3-4 independent experiments. e Gene ontology (GO) term enrichment analysis showing pathways related to inflammation that are significantly altered between senescent control (Sen siScr; n = 4 independent experiments) and senescent cells lacking MAVS (Sen siMAVS; n = 4 independent experiments). f The GSEA plots for Sen siScr and Sen siMAVS show an enrichment of SenMayo and SenSign genes in senescent control cells. g Column-clustered heatmap of cell-cycle genes upregulated in senescent cells and not changed by MAVS siRNA knockdown. Color intensity represents the column z-score. n = 3–4 independent experiments.

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