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Brain Protein Synthesis and Cell Proliferation in Sulfur Amino Acid Restricted Mice
Author(s) -
Martinez Wenceslao,
Zhang Qian,
Mirek Emily,
Levy Jordan,
Jonsson William,
Anthony Tracy,
Hamilton Karyn
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.05183
Subject(s) - proteostasis , biology , proteome , microbiology and biotechnology , protein biosynthesis , protein degradation , cell growth , cytosol , biochemistry , medicine , enzyme
Protein homeostasis (proteostasis) is the maintenance of the proteome through cellular pathways that are involved in protein synthesis, folding, trafficking, and degradation. Loss of proteostasis is considered one of the hallmarks of aging, and is a driver for age‐related neurodegenerative diseases. In order to conserve healthy brain function throughout the lifespan, proteostasis must be maintained. We previously reported that dietary sulfur amino acid restriction (SAAR), a life‐/healthspan extending treatment, activates mechanisms that maintain proteostasis in the liver. However, it is unknown if SAAR activates mechanisms promoting proteostatic maintenance in the brain. To address this knowledge gap, wild‐type male C57Bl/B6 mice were fed one of four diets: Regular fat control, regular fat SAAR, high fat control, and high fat SAAR. Mice consumed deuterium enriched water, which was used to measure long term rates of newly synthesized proteins and DNA. Brains were collected at days 1, 3, 7, 14, 21, and 35 of treatment. Mitochondrial, cytosolic, and mixed fractions of pulverized frontal cortex were analyzed for rates of protein synthesis and cell proliferation using GC/MS. Data collection is ongoing, however based on preliminary and previous studies analyzing liver and brain, we anticipate that under SAAR, protein synthesis rates will be maintained in select tissue fractions despite slower rates of cell proliferation compared to mice without SAAR.