PERFORM Publications

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Title		Authors	PubMed ID
1	Diverse geroprotectors differently affect a mechanism linking cellular aging to cellular quiescence in budding yeast	Leonov A; Feldman R; Piano A; Arlia-Ciommo A; Junio JAB; Orfanos E; Tafakori T; Lutchman V; Mohammad K; Elsaser S; Orfali S; Rajen H; Titorenko VI;	35937500 BIOLOGY
2	Empowering Melatonin Therapeutics with Drosophila Models	Millet-Boureima C; Ennis CC; Jamison J; McSweeney S; Park A; Gamberi C;	34698120 BIOLOGY
3	Cyst Reduction by Melatonin in a Novel Drosophila Model of Polycystic Kidney Disease.	Millet-Boureima C; Rozencwaig R; Polyak F; Gamberi C;	33238462 BIOLOGY
4	Discovery of fifteen new geroprotective plant extracts and identification of cellular processes they affect to prolong the chronological lifespan of budding yeast.	Dakik P, Rodriguez MEL, Junio JAB, Mitrofanova D, Medkour Y, Tafakori T, Taifour T, Lutchman V, Samson E, Arlia-Ciommo A, Rukundo B, Simard É, Titorenko VI	32577164 BIOLOGY
5	Lithocholic bile acid accumulated in yeast mitochondria orchestrates a development of an anti-aging cellular pattern by causing age-related changes in cellular proteome.	Beach A, Richard VR, Bourque S, Boukh-Viner T, Kyryakov P, Gomez-Perez A, Arlia-Ciommo A, Feldman R, Leonov A, Piano A, Svistkova V, Titorenko VI	25839782 MASSSPEC
6	Some Metabolites Act as Second Messengers in Yeast Chronological Aging.	Mohammad K, Dakik P, Medkour Y, McAuley M, Mitrofanova D, Titorenko VI	29543708 BIOLOGY

Title:	Lithocholic bile acid accumulated in yeast mitochondria orchestrates a development of an anti-aging cellular pattern by causing age-related changes in cellular proteome.
Authors:	Beach A, Richard VR, Bourque S, Boukh-Viner T, Kyryakov P, Gomez-Perez A, Arlia-Ciommo A, Feldman R, Leonov A, Piano A, Svistkova V, Titorenko VI
Link:	https://www.ncbi.nlm.nih.gov/pubmed/25839782?dopt=Abstract
DOI:	10.1080/15384101.2015.1026493
Publication:	Cell cycle (Georgetown, Tex.)
Keywords:	D, diauxic growth phase; DMSO, dimethyl sulfoxide; ER, endoplasmic reticulum; ETC, electron transport chain; ISC, iron-sulfur clusters; LCA, lithocholic acid; MAM, mitochondria-associated membrane; OS, oxidative stress; PD, post-diauxic growth phase; PMD, partial mitochondrial dysfunction; ROS, reactive oxygen species; ST, stationary growth phase; TCA, tricarboxylic acid; WT, wild type; anti-aging compounds; cell metabolism; cellular aging; lithocholic bile acid; longevity; mitochondria; mitochondrial proteome; mitochondrial signaling; signal transduction; yeast;
PMID:	25839782	Category:	Cell Cycle	Date Added:	2019-06-20
Dept Affiliation:	MASSSPEC 1 a Department of Biology; Concordia University ; Montreal , QC , Canada.

Description:

Lithocholic bile acid accumulated in yeast mitochondria orchestrates a development of an anti-aging cellular pattern by causing age-related changes in cellular proteome.

Cell Cycle. 2015;14(11):1643-56

Authors: Beach A, Richard VR, Bourque S, Boukh-Viner T, Kyryakov P, Gomez-Perez A, Arlia-Ciommo A, Feldman R, Leonov A, Piano A, Svistkova V, Titorenko VI

Abstract

We have previously revealed that exogenously added lithocholic bile acid (LCA) extends the chronological lifespan of the yeast Saccharomyces cerevisiae, accumulates in mitochondria and alters mitochondrial membrane lipidome. Here, we use quantitative mass spectrometry to show that LCA alters the age-related dynamics of changes in levels of many mitochondrial proteins, as well as numerous proteins in cellular locations outside of mitochondria. These proteins belong to 2 regulons, each modulated by a different mitochondrial dysfunction; we call them a partial mitochondrial dysfunction regulon and an oxidative stress regulon. We found that proteins constituting these regulons (1) can be divided into several "clusters", each of which denotes a distinct type of partial mitochondrial dysfunction that elicits a different signaling pathway mediated by a discrete set of transcription factors; (2) exhibit 3 different patterns of the age-related dynamics of changes in their cellular levels; and (3) are encoded by genes whose expression is regulated by the transcription factors Rtg1p/Rtg2p/Rtg3p, Sfp1p, Aft1p, Yap1p, Msn2p/Msn4p, Skn7p and Hog1p, each of which is essential for longevity extension by LCA. Our findings suggest that LCA-driven changes in mitochondrial lipidome alter mitochondrial proteome and functionality, thereby enabling mitochondria to operate as signaling organelles that orchestrate an establishment of an anti-aging transcriptional program for many longevity-defining nuclear genes. Based on these findings, we propose a model for how such LCA-driven changes early and late in life of chronologically aging yeast cause a stepwise development of an anti-aging cellular pattern and its maintenance throughout lifespan.

PMID: 25839782 [PubMed - indexed for MEDLINE]

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