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Projekt Druckansicht

Der Proteinhomöostase-Metabolismus Wechselwirkung als Schutz der zellulären Langlebigkeit

Antragstellerin Dr. Anita Krisko
Fachliche Zuordnung Zellbiologie
Biochemie
Stoffwechselphysiologie, Biochemie und Genetik der Mikroorganismen
Förderung Förderung von 2020 bis 2024
Projektkennung Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 443310721
 
Erstellungsjahr 2024

Zusammenfassung der Projektergebnisse

Aging is a natural phenomenon characterized by a progressive decline despite complex pathways of maintenance and repair. The loss of proteostasis in aging results in the inability of proteins to achieve and maintain their native three-dimensional structure and perform their functions efficiently. To counteract this, cells have evolved mechanisms to promote the removal of damaged proteins through degradation and nucleation and growth of protein aggregates. The functions of protein refolding, targeting to degradation and aggregate nucleation are all performed by molecular chaperones. Using budding yeast S. cerevisiae as a model system, we investigated how changes in proteostasis affect protein condensation, modulate metabolic pathway activity and extend lifespan. Our study reveals a previously unknown role of Hsp42 in SG dynamics during the response to glucose starvation. We found that SG formation and dissolution are stepwise processes in wild- type cells, involving fusion and fission events, respectively. Notably, this phenotype is attributed to the N-terminal domain of Hsp42. Moreover, our results show that the absence of Hsp42 leads to an extension of yeast replicative lifespan (RLS) that requires a switch to respiratory metabolism, despite the abundance of glucose, accompanied by a decline in glucose uptake. These results illustrate dynamic communication between proteostasis, metabolism and lifespan driven by Hsp42 deficiency.

Projektbezogene Publikationen (Auswahl)

 
 

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