Biochemical properties and excretion behavior of repressible acid phosphatases with altered subunit composition

Shnyreva, Maria; Петрова, Е. В.; Egorov, S. N.; Hinnen, Albert

doi:10.1016/s0944-5013(96)80027-9

Cited by 17 publications

(7 citation statements)

References 13 publications

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“…1B and Dataset S2), suggesting that they were posttranslationally modified or in an SDS-resistant aggregated form. Consistent with this idea, Pho11 and Pho5 are glycoproteins and known to run aberrantly on SDS/PAGE (21), and Pma1 and Mrh1 are integral membrane proteins and are modified or prone to aggregation (22).…”

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confidence: 79%

Identification of long-lived proteins retained in cells undergoing repeated asymmetric divisions

Thayer

Leverich

Fitzgibbon

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Long-lived proteins have been implicated in age-associated decline in metazoa, but they have only been identified in extracellular matrices or postmitotic cells. However, the aging process also occurs in dividing cells undergoing repeated asymmetric divisions. It was not clear whether long-lived proteins exist in asymmetrically dividing cells or whether they are involved in aging. Here we identify long-lived proteins in dividing cells during aging using the budding yeast, Saccharomyces cerevisiae. Yeast mother cells undergo a limited number of asymmetric divisions that define replicative lifespan. We used stable-isotope pulse-chase and total proteome mass-spectrometry to identify proteins that were both long-lived and retained in aging mother cells after ∼18 cells divisions. We identified ∼135 proteins that we designate as long-lived asymmetrically retained proteins (LARPS). Surprisingly, the majority of LARPs appeared to be stable fragments of their original fulllength protein. However, 15% of LARPs were full-length proteins and we confirmed several candidates to be long-lived and retained in mother cells by time-lapse microscopy. Some LARPs localized to the plasma membrane and remained robustly in the mother cell upon cell division. Other full-length LARPs were assembled into large cytoplasmic structures that had a strong bias to remain in mother cells. We identified age-associated changes to LARPs that include an increase in their levels during aging because of their continued synthesis, which is not balanced by turnover. Additionally, several LARPs were posttranslationally modified during aging. We suggest that LARPs contribute to age-associated phenotypes and likely exist in other organisms.ACD | asymmetric cell division | RITE | recombination-induced tag exchange | replicative aging

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mentioning

confidence: 79%

Identification of long-lived proteins retained in cells undergoing repeated asymmetric divisions

Thayer

Leverich

Fitzgibbon

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…Regardless, it was recently shown that Cdk1 can phosphorylate the transcription factor Pho2 on S230, resulting in increased binding of Pho2 to Pho4 [160]. The Pho2-Pho4 complex is required for activation of PHO5 , which encodes an acid phosphatase that is secreted into the periplasmic space and scavenges phosphate by working in conjunction with high-affinity phosphate transporters [161]. Pho2 also associates with the Myb-like transcription factor Bas1 to activate genes in the pyrimidine, purine and histidine biosynthesis pathways [162].…”

Section: Processes and Targets Controlled By Cdk1mentioning

confidence: 99%

An overview of Cdk1-controlled targets and processes

2010

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The cyclin dependent kinase Cdk1 controls the cell cycle, which is best understood in the model organism S. cerevisiae. Research performed during the past decade has significantly improved our understanding of the molecular machinery of the cell cycle. Approximately 75 targets of Cdk1 have been identified that control critical cell cycle events, such as DNA replication and segregation, transcriptional programs and cell morphogenesis. In this review we discuss currently known targets of Cdk1 in the budding yeast S. cerevisiae and highlight the role of Cdk1 in several crucial processes including maintenance of genome stability.

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“…These observations led to the suggestion that the chromosome I genes could be repressed by a TPE (Barton et al 1997). The endmost chromosome I ORFs are YAR073W/IMD1, encoding an IMP dehydrogenase ortholog (Hyle et al 2003); YAR071W/PHO11, encoding an inducible acid phosphatase (Kaback et al 1989;Shnyreva et al 1996); and YAR068W, encoding a nonessential putative membrane protein of unknown function that when overexpressed produces a drug-resistance phenotype (Barton et al 1997;Launhardt et al 1998).…”

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confidence: 99%