Kinetics of Formation and Asymmetrical Distribution of Hsp104-Bound Protein Aggregates in Yeast.

Biophys J

Development and Stem Cells Department, IGBMC, CNRS UMR 7104, INSERM U964, Université de Strasbourg, Illkirch, France. Electronic address:

Published: April 2016

Budding yeast cells have a finite replicative life span; that is, a mother cell produces only a limited number of daughter cells before it slows division and dies. Despite the gradual aging of the mother cell, all daughters are born rejuvenated and enjoy a full replicative lifespan. It has been proposed that entry of mother cells into senescence is driven by the progressive accumulation and retention of damaged material, including protein aggregates. This additionally allows the daughter cells to be born damage free. However, the mechanism underlying such asymmetrical segregation of protein aggregates by mother and daughter cells remains controversial, in part because of the difficulties inherent in tracking the dynamics and fate of protein aggregates in vivo. To overcome such limitations, we have developed single-cell real-time imaging methodology to track the formation of heat-induced protein aggregates in otherwise unperturbed dividing cells. By combining the imaging data with a simple computational model of protein aggregation, we show that the establishment of asymmetrical partitioning of protein aggregates upon division is driven by the large bud-specific dilution rate associated with polarized growth and the absence of significant mother/bud exchange of protein aggregates during the budded phase of the cell cycle. To our knowledge, this study sheds new light on the mechanism of establishment of a segregation bias, which can be accounted for by simple physical arguments.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4833780PMC
http://dx.doi.org/10.1016/j.bpj.2016.02.034DOI Listing

Publication Analysis

Top Keywords

protein aggregates
28
daughter cells
12
protein
8
mother cell
8
aggregates
7
cells
6
kinetics formation
4
formation asymmetrical
4
asymmetrical distribution
4
distribution hsp104-bound
4

Similar Publications

A point mutation in a like gene in enhances the anticorrosion activity.

Appl Environ Microbiol

January 2025

Key Laboratory for Water Quality and Conservation of the Pearl River Delta, Ministry of Education, School of Environmental Science and Engineering, Guangzhou University, Guangzhou, China.

The protection of steel based on microbial biomineralization has emerged as a novel and eco-friendly strategy for corrosion control. However, the molecular basis of the biomineralization process in mineralization bacteria remains largely unexplored. We previously reported that EPS+ strain provides protection against steel corrosion by forming a hybrid biomineralization film.

View Article and Find Full Text PDF

Tracing TMEM106B fibril deposition in aging and Parkinson's disease with dementia brains.

Life Med

February 2024

Department of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai 200040, China.

Transmembrane protein 106B (TMEM106B), previously identified as a risk factor in frontotemporal lobar degeneration, has recently been detected to form fibrillar aggregates in the brains of patients with various neurodegenerative diseases (NDs) and normal elders. While the specifics of when and where TMEM106B fibrils accumulate in human brains, as well as their connection to aging and disease progression, remain poorly understood. Here, we identified an antibody (NBP1-91311) that directly binds to TMEM106B fibrils extracted from the brain and to Thioflavin S-positive TMEM106B fibrillar aggregates in brain sections.

View Article and Find Full Text PDF

The three-dimensional structure of proteins, achieved through the folding of the nascent polypeptide chain in vivo, is largely facilitated by molecular chaperones, which are crucial for determining protein functionality. In addition to aiding in the folding process, chaperones target misfolded proteins for degradation, acting as a quality control system within the cell. Defective protein folding has been implicated in a wide range of clinical conditions, including neurodegenerative and metabolic disorders.

View Article and Find Full Text PDF

Tau oligomers impair memory and synaptic plasticity through the cellular prion protein.

Acta Neuropathol Commun

January 2025

Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy.

Deposition of abnormally phosphorylated tau aggregates is a central event leading to neuronal dysfunction and death in Alzheimer's disease (AD) and other tauopathies. Among tau aggregates, oligomers (TauOs) are considered the most toxic. AD brains show significant increase in TauOs compared to healthy controls, their concentration correlating with the severity of cognitive deficits and disease progression.

View Article and Find Full Text PDF

Impact of Weak Vibration Generated by a Refrigerator on Protein Aggregation.

AAPS J

January 2025

Department of Biotechnology, Graduate School of Engineering, Osaka University, 2-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.

Protein aggregates and particles in biopharmaceuticals can induce adverse immune responses in patients. Thus, suppression of the formation of protein aggregates and particles is important for the successful development of therapeutic proteins. Mechanical stresses, including agitation, are widely recognized as stress factors that generate protein aggregates and particles.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!