CCR4-NOT complex in stress resistance and longevity in C. elegans

“[...] it appears that the CCR4-NOT complex can influence longevity in a multitude of manners [...]”

BUFFALO, NY- June 11, 2024 – A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “CCR4-NOT complex in stress resistance and longevity in C. elegans.”

The ability to mount an adaptive response to environmental stress is crucial in organismal survival and overall fitness. In the context of aging, many genes that mediate resistance to stressors are also important in longevity, and aging has been shown to cause a decline in stress resistance. In their new editorial, researchers Cheng-Wei Wu and Hadi Tabarraei from the University of Saskatchewan wrote that recently, during a screening for genes that are required for the transcriptional response to heavy metal and oxidative stress in C. elegans, they found that depletion of subunits within the evolutionarily conserved CCR4-NOT protein complex compromises stress resistance and decreases lifespan.

“The CCR4-NOT (Carbon Catabolite Repression 4 – Negative On TATA-less) is a multi-protein complex tasked with regulating RNA metabolism across multiple steps including mRNA decay, transcription initiation and elongation, mRNA quality control and export, and mRNA translatability (reviewed in [3]).”

Studies in yeast have shown that CCR4-NOT is required for transcriptional elongation of stress responsive genes and that loss of function mutants of this protein complex have increased sensitivity to replication stress caused by DNA damaging agents [4, 5]. An expansive role for the CCR4-NOT complex in stress-induced transcriptional programming was demonstrated in C. elegans via whole-transcriptome sequencing analysis [2]. 

“Together, while the CCR4-NOT complex has been extensively studied for the past 3 decades, new studies in the model organism C. elegans have revealed an important new role for this protein complex in regulating normal aging as well as a requirement for many well-characterized and evolutionarily conserved pro-longevity pathways including reduced insulin signaling, mitochondrial suppression, enhanced stress response, and dietary restriction.”

Read the full paper: DOI: https://doi.org/10.18632/aging.205918 

Corresponding Author: Cheng-Wei Wu

Corresponding Email: michael.wu@usask.ca 

Keywords: aging, oxidative stress, C. elegans, CCR4-NOT

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About Aging:

Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.

Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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