scholarly journals Heat stress promotes longevity in budding yeast by relaxing the confinement of age-promoting factors in the mother cell

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Sandro Baldi ◽  
Alessio Bolognesi ◽  
Anne Cornelis Meinema ◽  
Yves Barral

Although individuals of many species inexorably age, a number of observations established that the rate of aging is modulated in response to a variety of mild stresses. Here, we investigated how heat stress promotes longevity in yeast. We show that upon growth at higher temperature, yeast cells relax the retention of DNA circles, which act as aging factors in the mother cell. The enhanced frequency at which circles redistribute to daughter cells was not due to changes of anaphase duration or nuclear shape but solely to the downregulation of the diffusion barrier in the nuclear envelope. This effect depended on the PKA and Tor1 pathways, downstream of stress-response kinase Pkc1. Inhibition of these responses restored barrier function and circle retention and abrogated the effect of heat stress on longevity. Our data indicate that redistribution of aging factors from aged cells to their progeny can be a mechanism for modulating longevity.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nelson Martínez-Matías ◽  
Nataliya Chorna ◽  
Sahily González-Crespo ◽  
Lilliam Villanueva ◽  
Ingrid Montes-Rodríguez ◽  
...  

AbstractFunctional analysis of the Mtl1 protein in Saccharomyces cerevisiae has revealed that this transmembrane sensor endows yeast cells with resistance to oxidative stress through a signaling mechanism called the cell wall integrity pathway (CWI). We observed upregulation of multiple heat shock proteins (HSPs), proteins associated with the formation of stress granules, and the phosphatase subunit of trehalose 6-phosphate synthase which suggests that mtl1Δ strains undergo intrinsic activation of a non-lethal heat stress response. Furthermore, quantitative global proteomic analysis conducted on TMT-labeled proteins combined with metabolome analysis revealed that mtl1Δ strains exhibit decreased levels of metabolites of carboxylic acid metabolism, decreased expression of anabolic enzymes and increased expression of catabolic enzymes involved in the metabolism of amino acids, with enhanced expression of mitochondrial respirasome proteins. These observations support the idea that Mtl1 protein controls the suppression of a non-lethal heat stress response under normal conditions while it plays an important role in metabolic regulatory mechanisms linked to TORC1 signaling that are required to maintain cellular homeostasis and optimal mitochondrial function.


2020 ◽  
Author(s):  
Yasmin Lau ◽  
Iuliia Parfenova ◽  
Juha Saarikangas ◽  
Richard A. Nichols ◽  
Yves Barral ◽  
...  

AbstractIn response to deceptive courtship, budding yeast cells escape pheromone induced cell cycle arrest through coalescence of the G1/S inhibitor Whi3 into a dominant inactive super-assembly. Strikingly, Whi3 super-assemblies remain stable over many cell cycles in the mother cells and are not passed on to the daughter cells. Thereby, Whi3 coalescence encodes memory, conferring to it the property of a mnemon (Whi3mnem), a protein which conformational change maintain a trait that is permanent in the mother cell but is not inherited by daughter cells. Mnemons share structural features with prions, which are self-templating protein conformations that are inherited by daughter cells. Yet, how the maintenance and asymmetric inheritance of Whi3mnem are achieved is unknown. Here, we report that Whi3mnem is closely associated with endoplasmic reticulum (ER) membranes and retained in the mother cell by the presence of lateral membrane diffusion barriers at the bud neck. Strikingly, barrier defects made Whi3mnem propagate in a mitotically stable manner, like a prion. Alike Whi3mnem, transformation of Whi3 into a prion required its poly-glutamine prion-like domain. Thus, we propose that Whi3mnem is in a self-templating state, lending temporal stability to the memory that it encodes, while its anchorage into the compartmentalized membranes of the ER ensures its confinement in the mother cell and prevents its infectious propagation. These results suggest that confined self-templating super-assembly is a powerful mechanism for the long-term encoding of information.


eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Lori Clay ◽  
Fabrice Caudron ◽  
Annina Denoth-Lippuner ◽  
Barbara Boettcher ◽  
Stéphanie Buvelot Frei ◽  
...  

In many cell types, lateral diffusion barriers compartmentalize the plasma membrane and, at least in budding yeast, the endoplasmic reticulum (ER). However, the molecular nature of these barriers, their mode of action and their cellular functions are unclear. Here, we show that misfolded proteins of the ER remain confined into the mother compartment of budding yeast cells. Confinement required the formation of a lateral diffusion barrier in the form of a distinct domain of the ER-membrane at the bud neck, in a septin-, Bud1 GTPase- and sphingolipid-dependent manner. The sphingolipids, but not Bud1, also contributed to barrier formation in the outer membrane of the dividing nucleus. Barrier-dependent confinement of ER stress into the mother cell promoted aging. Together, our data clarify the physical nature of lateral diffusion barriers in the ER and establish the role of such barriers in the asymmetric segregation of proteotoxic misfolded proteins during cell division and aging.


Genetics ◽  
2002 ◽  
Vol 162 (1) ◽  
pp. 73-87 ◽  
Author(s):  
Chi-Yung Lai ◽  
Ewa Jaruga ◽  
Corina Borghouts ◽  
S Michal Jazwinski

Abstract The yeast Saccharomyces cerevisiae reproduces by asymmetric cell division, or budding. In each cell division, the daughter cell is usually smaller and younger than the mother cell, as defined by the number of divisions it can potentially complete before it dies. Although individual yeast cells have a limited life span, this age asymmetry between mother and daughter ensures that the yeast strain remains immortal. To understand the mechanisms underlying age asymmetry, we have isolated temperature-sensitive mutants that have limited growth capacity. One of these clonal-senescence mutants was in ATP2, the gene encoding the β-subunit of mitochondrial F1, F0-ATPase. A point mutation in this gene caused a valine-to-isoleucine substitution at the ninetieth amino acid of the mature polypeptide. This mutation did not affect the growth rate on a nonfermentable carbon source. Life-span determinations following temperature shift-down showed that the clonal-senescence phenotype results from a loss of age asymmetry at 36°, such that daughters are born old. It was characterized by a loss of mitochondrial membrane potential followed by the lack of proper segregation of active mitochondria to daughter cells. This was associated with a change in mitochondrial morphology and distribution in the mother cell and ultimately resulted in the generation of cells totally lacking mitochondria. The results indicate that segregation of active mitochondria to daughter cells is important for maintenance of age asymmetry and raise the possibility that mitochondrial dysfunction may be a normal cause of aging. The finding that dysfunctional mitochondria accumulated in yeasts as they aged and the propensity for old mother cells to produce daughters depleted of active mitochondria lend support to this notion. We propose, more generally, that age asymmetry depends on partition of active and undamaged cellular components to the progeny and that this “filter” breaks down with age.


2017 ◽  
Author(s):  
Xi Lan ◽  
John C. F. Hsieh ◽  
Carl J. Schmidt ◽  
Qing Zhu ◽  
Susan J. Lamont

2016 ◽  
Vol 22 (18) ◽  
pp. 2619-2639 ◽  
Author(s):  
Biljana Miova ◽  
Maja Dimitrovska ◽  
Suzana Dinevska-Kjovkarovska ◽  
Juan V. Esplugues ◽  
Nadezda Apostolova

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bin Huang ◽  
Zhinuo Huang ◽  
Ruifang Ma ◽  
Jialu Chen ◽  
Zhijun Zhang ◽  
...  

AbstractHeat shock transcription factors (HSFs) are central elements in the regulatory network that controls plant heat stress response. They are involved in multiple transcriptional regulatory pathways and play important roles in heat stress signaling and responses to a variety of other stresses. We identified 41 members of the HSF gene family in moso bamboo, which were distributed non-uniformly across its 19 chromosomes. Phylogenetic analysis showed that the moso bamboo HSF genes could be divided into three major subfamilies; HSFs from the same subfamily shared relatively conserved gene structures and sequences and encoded similar amino acids. All HSF genes contained HSF signature domains. Subcellular localization prediction indicated that about 80% of the HSF proteins were located in the nucleus, consistent with the results of GO enrichment analysis. A large number of stress response–associated cis-regulatory elements were identified in the HSF upstream promoter sequences. Synteny analysis indicated that the HSFs in the moso bamboo genome had greater collinearity with those of rice and maize than with those of Arabidopsis and pepper. Numerous segmental duplicates were found in the moso bamboo HSF gene family. Transcriptome data indicated that the expression of a number of PeHsfs differed in response to exogenous gibberellin (GA) and naphthalene acetic acid (NAA). A number of HSF genes were highly expressed in the panicles and in young shoots, suggesting that they may have functions in reproductive growth and the early development of rapidly-growing shoots. This study provides fundamental information on members of the bamboo HSF gene family and lays a foundation for further study of their biological functions in the regulation of plant responses to adversity.


2003 ◽  
Vol 26 (5) ◽  
pp. 701-708 ◽  
Author(s):  
Naoki Harikai ◽  
Kanji Tomogane ◽  
Mitsue Miyamoto ◽  
Keiko Shimada ◽  
Satoshi Onodera ◽  
...  

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