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Article

The Molecular Floodgates of Stress-Induced Senescence Reveal Translation, Signalling and Protein Activity Central to the Post-Mortem Proteome

1
Bioanalytical Mass Spectrometry Facility, Mark Wainwright Analytical Centre, University of New South Wales Sydney, Kensington, NSW 2052, Australia
2
Palaeontology, Geobiology and Earth Archives Research Centre, University of New South Wales Sydney, Kensington, NSW 2052, Australia
3
ARC Centre of Excellence for Australian Biodiversity and Heritage, University of New South Wales Sydney, Kensington, NSW 2052, Australia
4
Centre for Global Archaeological Research, University Sains Malaysia, Penang 11800, Malaysia
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(17), 6422; https://doi.org/10.3390/ijms21176422
Received: 22 July 2020 / Revised: 27 August 2020 / Accepted: 31 August 2020 / Published: 3 September 2020
The transitioning of cells during the systemic demise of an organism is poorly understood. Here, we present evidence that organismal death is accompanied by a common and sequential molecular flood of stress-induced events that propagate the senescence phenotype, and this phenotype is preserved in the proteome after death. We demonstrate activation of “death” pathways involvement in diseases of ageing, with biochemical mechanisms mapping onto neurological damage, embryonic development, the inflammatory response, cardiac disease and ultimately cancer with increased significance. There is sufficient bioavailability of the building blocks required to support the continued translation, energy, and functional catalytic activity of proteins. Significant abundance changes occur in 1258 proteins across 1 to 720 h post-mortem of the 12-week-old mouse mandible. Protein abundance increases concord with enzyme activity, while mitochondrial dysfunction is evident with metabolic reprogramming. This study reveals differences in protein abundances which are akin to states of stress-induced premature senescence (SIPS). The control of these pathways is significant for a large number of biological scenarios. Understanding how these pathways function during the process of cellular death holds promise in generating novel solutions capable of overcoming disease complications, maintaining organ transplant viability and could influence the findings of proteomics through “deep-time” of individuals with no historically recorded cause of death. View Full-Text
Keywords: death; coordinated gene-expression; ribosomal binding proteins; paleoproteomics; post-mortem; senescence; mitochondrial dysfunction; inflammation death; coordinated gene-expression; ribosomal binding proteins; paleoproteomics; post-mortem; senescence; mitochondrial dysfunction; inflammation
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MDPI and ACS Style

Wasinger, V.C.; Curnoe, D.; Boel, C.; Machin, N.; Goh, H.M. The Molecular Floodgates of Stress-Induced Senescence Reveal Translation, Signalling and Protein Activity Central to the Post-Mortem Proteome. Int. J. Mol. Sci. 2020, 21, 6422. https://doi.org/10.3390/ijms21176422

AMA Style

Wasinger VC, Curnoe D, Boel C, Machin N, Goh HM. The Molecular Floodgates of Stress-Induced Senescence Reveal Translation, Signalling and Protein Activity Central to the Post-Mortem Proteome. International Journal of Molecular Sciences. 2020; 21(17):6422. https://doi.org/10.3390/ijms21176422

Chicago/Turabian Style

Wasinger, Valerie C., Darren Curnoe, Ceridwen Boel, Naomi Machin, and Hsiao M. Goh 2020. "The Molecular Floodgates of Stress-Induced Senescence Reveal Translation, Signalling and Protein Activity Central to the Post-Mortem Proteome" International Journal of Molecular Sciences 21, no. 17: 6422. https://doi.org/10.3390/ijms21176422

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