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Journal articles on the topic 'Yeast mitochondrial escape'

Author: Grafiati

Published: 6 September 2023

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1

Campbell, C. L., and P. E. Thorsness. "Escape of mitochondrial DNA to the nucleus in yme1 yeast is mediated by vacuolar-dependent turnover of abnormal mitochondrial compartments." Journal of Cell Science 111, no. 16 (1998): 2455–64. http://dx.doi.org/10.1242/jcs.111.16.2455.

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Inactivation of Yme1p, a mitochondrially-localized ATP-dependent metallo-protease in the yeast Saccharomyces cerevisiae, causes a high rate of DNA escape from mitochondria to the nucleus as well as pleiotropic functional and morphological mitochondrial defects. The evidence presented here suggests that the abnormal mitochondria of a yme1 strain are degraded by the vacuole. First, electron microscopy of Yme1p-deficient strains revealed mitochondria physically associated with the vacuole via electron dense structures. Second, disruption of vacuolar function affected the frequency of mitochondria

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2

Hanekamp, T., and P. E. Thorsness. "Inactivation of YME2/RNA12, which encodes an integral inner mitochondrial membrane protein, causes increased escape of DNA from mitochondria to the nucleus in Saccharomyces cerevisiae." Molecular and Cellular Biology 16, no. 6 (1996): 2764–71. http://dx.doi.org/10.1128/mcb.16.6.2764.

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Inactivation of the yeast nuclear gene YMe2 causes an increased rate of DNA escape from mitochondria to the nucleus. Mutations in yme2 also show genetic interactions with yme1, a second gene that affects DNA escape from mitochondria to the nucleus. The yme1 cold-sensitive growth phenotype is suppressed by yme2 mutations. In addition, yme1 yme2 double mutants exhibit a synthetic growth defect on ethanol-glycerol medium at 30 degrees C. YME2 was isolated by complementation of the synthetic growth defect of yme1 yme2 strains and was found to be identical with the previously cloned RNA12 gene. The

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3

Thorsness, P. E., K. H. White, and T. D. Fox. "Inactivation of YME1, a member of the ftsH-SEC18-PAS1-CDC48 family of putative ATPase-encoding genes, causes increased escape of DNA from mitochondria in Saccharomyces cerevisiae." Molecular and Cellular Biology 13, no. 9 (1993): 5418–26. http://dx.doi.org/10.1128/mcb.13.9.5418-5426.1993.

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The yeast nuclear gene YME1 was one of six genes recently identified in a screen for mutations that elevate the rate at which DNA escapes from mitochondria and migrates to the nucleus. yme1 mutations, including a deletion, cause four known recessive phenotypes: an elevation in the rate at which copies of TRP1 and ARS1, integrated into the mitochondrial genome, escape to the nucleus; a heat-sensitive respiratory-growth defect; a cold-sensitive growth defect on rich glucose medium; and synthetic lethality in rho- (cytoplasmic petite) cells. The cloned YME1 gene complements all of these phenotype

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4

Thorsness, P. E., K. H. White, and T. D. Fox. "Inactivation of YME1, a member of the ftsH-SEC18-PAS1-CDC48 family of putative ATPase-encoding genes, causes increased escape of DNA from mitochondria in Saccharomyces cerevisiae." Molecular and Cellular Biology 13, no. 9 (1993): 5418–26. http://dx.doi.org/10.1128/mcb.13.9.5418.

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The yeast nuclear gene YME1 was one of six genes recently identified in a screen for mutations that elevate the rate at which DNA escapes from mitochondria and migrates to the nucleus. yme1 mutations, including a deletion, cause four known recessive phenotypes: an elevation in the rate at which copies of TRP1 and ARS1, integrated into the mitochondrial genome, escape to the nucleus; a heat-sensitive respiratory-growth defect; a cold-sensitive growth defect on rich glucose medium; and synthetic lethality in rho- (cytoplasmic petite) cells. The cloned YME1 gene complements all of these phenotype

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5

Weber, E. R., T. Hanekamp, and P. E. Thorsness. "Biochemical and functional analysis of the YME1 gene product, an ATP and zinc-dependent mitochondrial protease from S. cerevisiae." Molecular Biology of the Cell 7, no. 2 (1996): 307–17. http://dx.doi.org/10.1091/mbc.7.2.307.

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Inactivation of YME1 in yeast causes several distinct phenotypes: an increased rate of DNA escape from mitochondria, temperature-sensitive growth on nonfermentable carbon sources, extremely slow growth when mitochondrial DNA is completely absent from the cell, and altered morphology of the mitochondrial compartment. The protein encoded by YME1, Yme1p, contains two highly conserved sequence elements, one implicated in the binding and hydrolysis of ATP, and the second characteristic of active site residues found in neutral, zinc-dependent proteases. Both the putative ATPase and zinc-dependent pr

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6

Thorsness, P. E., and T. D. Fox. "Nuclear mutations in Saccharomyces cerevisiae that affect the escape of DNA from mitochondria to the nucleus." Genetics 134, no. 1 (1993): 21–28. http://dx.doi.org/10.1093/genetics/134.1.21.

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Abstract We have inserted a yeast nuclear DNA fragment bearing the TRP1 gene and its associated origin of DNA replication, ARS1, into the functional mitochondrial chromosome of a strain carrying a chromosomal trp1 deletion. TRP1 was not phenotypically expressed within the organelle. However, this Trp- strain readily gave rise to respiratory competent Trp+ clones that contained the TRP1/ARS1 fragment, associated with portions of mitochondrial DNA (mtDNA), replicating in their nuclei. Thus the Trp+ clones arose as a result of DNA escaping from mitochondria and migrating to the nucleus. We have i

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7

Shafer, Karen S., Theodor Hanekamp, Karen H. White, and Peter E. Thorsness. "Mechanisms of mitochondrial DNA escape to the nucleus in the yeast Saccharomyces cerevisiae." Current Genetics 36, no. 4 (1999): 183–94. http://dx.doi.org/10.1007/s002940050489.

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8

Fischer, Manuel, Sebastian Horn, Anouar Belkacemi, et al. "Protein import and oxidative folding in the mitochondrial intermembrane space of intact mammalian cells." Molecular Biology of the Cell 24, no. 14 (2013): 2160–70. http://dx.doi.org/10.1091/mbc.e12-12-0862.

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Oxidation of cysteine residues to disulfides drives import of many proteins into the intermembrane space of mitochondria. Recent studies in yeast unraveled the basic principles of mitochondrial protein oxidation, but the kinetics under physiological conditions is unknown. We developed assays to follow protein oxidation in living mammalian cells, which reveal that import and oxidative folding of proteins are kinetically and functionally coupled and depend on the oxidoreductase Mia40, the sulfhydryl oxidase augmenter of liver regeneration (ALR), and the intracellular glutathione pool. Kinetics o

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9

Wang, Yawen, Shuai Zhang, Yi Tang, and Youxiang Diao. "Screening of Duck Tembusu Virus NS3 Interacting Host Proteins and Identification of Its Specific Interplay Domains." Viruses 11, no. 8 (2019): 740. http://dx.doi.org/10.3390/v11080740.

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NS3 protein is a member of the non-structural protein of duck Tembusu virus (DTMUV), which contains three domains, each of which has serine protease, nucleotide triphosphatase, and RNA helicase activities, respectively. It performs a variety of biological functions that are involved in the regulation of the viral life cycle and host immune response. Based on the yeast two-hybrid system, we successfully transformed pGBKT7-NS3 bait plasmid into Y2H Gold, tested it to prove that it has no self-activation and toxicity, and then hybridized it with the prey yeast strain of the duck embryo fibroblast

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10

Cui, Yixian, Shanke Zhao, Zhihao Wu, Pinghua Dai, and Bing Zhou. "Mitochondrial release of the NADH dehydrogenase Ndi1 induces apoptosis in yeast." Molecular Biology of the Cell 23, no. 22 (2012): 4373–82. http://dx.doi.org/10.1091/mbc.e12-04-0281.

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Saccharomyces cerevisiae NDI1 codes for the internal mitochondrial ubiquinone oxidoreductase, which transfers electrons from NADH to ubiquinone in the respiratory chain. Previously we found that Ndi1 is a yeast homologue of the protein apoptosis-inducing factor–homologous mitochondrion-associated inducer of death and displays potent proapoptotic activity. Here we show that S. cerevisiae NDI1 is involved in apoptosis induced by various stimuli tested, including H2O2, Mn, and acetate acid, independent of Z-VAD-fmk (a caspase inhibitor) inhibition. Although Ndi1 also participates in respiration,

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11

De Luca, Veronica, Manuela Leo, Elisabetta Cretella, et al. "Role of yUbp8 in Mitochondria and Hypoxia Entangles the Finding of Human Ortholog Usp22 in the Glioblastoma Pseudo-Palisade Microlayer." Cells 11, no. 10 (2022): 1682. http://dx.doi.org/10.3390/cells11101682.

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KAT Gcn5 and DUB Ubp8 are required for respiration and mitochondria functions in budding yeast, and in this study we show that loss of respiratory activity is acquired over time. Interestingly, we show that absence of Ubp8 allows cells to grow in hypoxic conditions with altered mitophagy. Comparatively, the aggressive glioblastoma (GBM) multiforme tumor shows survival mechanisms able to overcome hypoxia in the brain. Starting from yeast and our findings on the role of Ubp8 in hypoxia, we extended our analysis to the human ortholog and signature cancer gene Usp22 in glioblastoma tumor specimens

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12

Toti, Florence, Bénédicte Hugel, Carole Gidon-Jeangirard, et al. "Apoptosis in Vascular Disease." Thrombosis and Haemostasis 82, no. 08 (1999): 727–35. http://dx.doi.org/10.1055/s-0037-1615904.

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IntroductionApoptosis, the term introduced 27 years ago to characterize a particular form of cell death distinct from necrosis,1 is now considered a genetically-controlled and energy-dependent process of fundamental significance in the development and maintenance of homeostasis in multicellular organisms.2-4 For instance, in the nematode Caenorhabditis elegans, a model widely used for the study of programmed cell death, 131 of the 1,090 somatic cells generated during hermaphrodite development undergo this form of death.5 Embryologists have suspected cell death of being instrumental in the “scu

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13

Newman, Laura E., and Gerald S. Shadel. "Mitochondrial DNA Release in Innate Immune Signaling." Annual Review of Biochemistry 92, no. 1 (2023). http://dx.doi.org/10.1146/annurev-biochem-032620-104401.

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According to the endosymbiotic theory, most of the DNA of the original bacterial endosymbiont has been lost or transferred to the nucleus, leaving a much smaller (∼16 kb in mammals), circular molecule that is the present-day mitochondrial DNA (mtDNA). The ability of mtDNA to escape mitochondria and integrate into the nuclear genome was discovered in budding yeast, along with genes that regulate this process. Mitochondria have emerged as key regulators of innate immunity, and it is now recognized that mtDNA released into the cytoplasm, outside of the cell, or into circulation activates multiple

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14

Tucey, Timothy M., Jiyoti Verma-Gaur, Julie Nguyen, et al. "The Endoplasmic Reticulum-Mitochondrion Tether ERMES Orchestrates Fungal Immune Evasion, Illuminating Inflammasome Responses to Hyphal Signals." mSphere 1, no. 3 (2016). http://dx.doi.org/10.1128/msphere.00074-16.

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ABSTRACT The yeast Candida albicans causes human infections that have mortality rates approaching 50%. The key to developing improved therapeutics is to understand the host-pathogen interface. A critical interaction is that with macrophages: intracellular Candida triggers the NLRP3/caspase-1 inflammasome for escape through lytic host cell death, but this also activates antifungal responses. To better understand how the inflammasome response to Candida is fine-tuned, we established live-cell imaging of inflammasome activation at single-cell resolution, coupled with analysis of the fungal ERMES

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15

Cui, Shuna, Minghui Li, Rabeay Y. A. Hassan, Anna Heintz-Buschart, Junsong Wang, and Ursula Bilitewski. "Inhibition of Respiration of Candida albicans by Small Molecules Increases Phagocytosis Efficacy by Macrophages." mSphere 5, no. 2 (2020). http://dx.doi.org/10.1128/msphere.00016-20.

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ABSTRACT Candida albicans adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These adaptive reactions not only allow survival but also influence the interaction with host cells, which is governed by the composition and structure of the fungal cell wall. Numerous studies had shown linkages between mitochondrial functionality, cell wall integrity and structure, and pathogenicity. Thus, we decided to inhibit single complexes of the respiratory chain of C. albicans and to analyze the resultant interaction with macrophages

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