Department of Biochemistry and Cell Biology, University of Rzeszow, Zelwerowicza 4, 35-601, Rzeszow, Poland.
Department of Cell Biology and Imaging, Institute of Zoology, Jagiellonian University, Krakow, Poland.
Biogerontology. 2018 Feb;19(1):67-79. doi: 10.1007/s10522-017-9740-6. Epub 2017 Nov 30.
The Saccharomyces cerevisiae yeast is one of the most widely used model in studies of cellular and organismal biology, including as aging and proliferation. Although several constraints of aging and budding lifespan have been identified, these processes have not yet been fully understood. Previous studies of aging in yeast have focused mostly on the molecular basics of the underlying mechanisms, while physical aspects, particularly those related to the cell wall, were rather neglected. In this paper, we examine for the first time, to our knowledge, the impact of cell wall biosynthesis disturbances on the lifespan in the budding yeast. We have used a set of cell wall mutants, including knr4Δ, cts1Δ, chs3Δ, fks1Δ and mnn9Δ, which affect biosynthesis of all major cell wall compounds. Our results indicated that impairment of chitin biosynthesis and cell wall protein mannosylation reduced the budding lifespan, while disruption in the 1,3-β-glucan synthase activity had no adverse effect on that parameter. The impact varied in the severity and the most notable effect was observed for the mnn9Δ mutant. What was interesting, in the case of the dysfunction of the Knr4 protein playing the role of the transcriptional regulator of cell wall chitin and glucan synthesis, the lifespan increased significantly. We also report the phenotypic characteristics of cell wall-associated mutants as revealed by imaging of the cell wall using transmission electron microscopy, scanning electron microscopy and atomic force microscopy. In addition, our findings support the conviction that achievement of the state of hypertrophy may not be the only factor that determines the budding lifespan.
酿酒酵母是细胞和机体生物学研究中最广泛使用的模型之一,包括衰老和增殖。尽管已经确定了衰老和出芽寿命的几个限制,但这些过程尚未完全理解。以前对酵母衰老的研究主要集中在潜在机制的分子基础上,而物理方面,特别是与细胞壁相关的方面,却被忽视了。在本文中,我们首次检查了,据我们所知,细胞壁生物合成紊乱对出芽酵母寿命的影响。我们使用了一组细胞壁突变体,包括 knr4Δ、cts1Δ、chs3Δ、fks1Δ 和 mnn9Δ,它们影响所有主要细胞壁化合物的生物合成。我们的结果表明,几丁质生物合成和细胞壁蛋白甘露糖基化的损伤降低了出芽寿命,而 1,3-β-葡聚糖合酶活性的破坏对该参数没有不利影响。这种影响在严重程度上有所不同,最显著的影响发生在 mnn9Δ突变体中。有趣的是,在 Knr4 蛋白作为细胞壁几丁质和葡聚糖合成的转录调节剂功能失调的情况下,寿命显著增加。我们还报告了细胞壁相关突变体的表型特征,这些特征是通过使用透射电子显微镜、扫描电子显微镜和原子力显微镜对细胞壁进行成像来揭示的。此外,我们的发现支持这样一种信念,即实现肥大状态可能不是决定出芽寿命的唯一因素。