Published, Version of Record (VoR)CC BY V4.0, Open
Abstract
Life Sciences & Biomedicine Science & Technology Physiology
Mitochondrial dysfunction activates intracellular signaling pathways that impact yeast longevity, and the best known of these pathways is the retrograde response. More recently, similar responses have been discerned in other systems, from invertebrates to human cells. However, the identity of the signal transducers is either unknown or apparently diverse, contrasting with the well-established signaling module of the yeast retrograde response. On the other hand, it has become equally clear that several other pathways and processes interact with the retrograde response, embedding it in a network responsive to a variety of cellular states. An examination of this network supports the notion that the master regulator NF kappa B aggregated a variety of mitochondria-related cellular responses at some point in evolution and has become the retrograde transcription factor. This has significant consequences for how we view some of the deficits associated with aging, such as inflammation. The support for NF kappa B as the retrograde response transcription factor is not only based on functional analyses. It is bolstered by the fact that NF kappa B can regulate Myc-Max, which is activated in human cells with dysfunctional mitochondria and impacts cellular metabolism. Myc-Max is homologous to the yeast retrograde response transcription factor Rtg1-Rtg3. Further research will be needed to disentangle the pro-aging from the anti-aging effects of NF kappa B. Interestingly, this is also a challenge for the complete understanding of the yeast retrograde response.
The yeast retrograde response as a model of intracellular signaling of rnitochondrial dysfunction
Creators
S. Michal Jazwinski - Tulane University
Andres Kriete - Drexel University
Publication Details
Frontiers in physiology, v 3, 139
Publisher
Frontiers Research Foundation
Number of pages
12
Grant note
R01AG000618 / NATIONAL INSTITUTE ON AGING; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute on Aging (NIA)
AG00618 / National Institutes of Health; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA
Wallace II. Coulter Foundation (Andres Kriete)
Resource Type
Journal article
Language
English
Academic Unit
School of Biomedical Engineering, Science, and Health Systems
Web of Science ID
WOS:000209173000136
Scopus ID
2-s2.0-84866409979
Other Identifier
991019168899104721
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