Evidence map›Paper›PMID 41068765›Full record

ArticleBMC biology2025

Proteasome regulation of petite-negativity in fission yeast.

Katie Lin Amberg, Lyrica Hao, Susanne Cranz-Mileva, Mikel Zaratiegui

Abstract read
In one paragraph

Article in BMC biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Katie Lin AmbergDepartment of Molecular Biology and Biochemistry, Division of Life Sciences, Rutgers, the State University of New Jersey, Piscataway, USA.
Lyrica HaoDepartment of Molecular Biology and Biochemistry, Division of Life Sciences, Rutgers, the State University of New Jersey, Piscataway, USA.
Susanne Cranz-MilevaDepartment of Molecular Biology and Biochemistry, Division of Life Sciences, Rutgers, the State University of New Jersey, Piscataway, USA.
Mikel ZaratieguiDepartment of Molecular Biology and Biochemistry, Division of Life Sciences, Rutgers, the State University of New Jersey, Piscataway, USA. zaratiegui@dls.rutgers.edu.

Funding

The cross-regulation of host DNA replication and LTR RetrotransposonsR35GM131763 · NIGMS · RUTGERS, THE STATE UNIV OF N.J. · PI ZARATIEGUI BIURRUN, MIGUEL ANGEL · 2019 to 2023
$2.0M
A Bruker timsTOF HT mass spectrometer and nanoflow LC system to upgrade the proteomics facility at Rutgers-New Brunswick and Robert Wood Johnson Medical SchoolS10OD036226 · OD · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI ZHENG, HAIYAN · 2024 to 2024
$1.1M
NIGMS NIH HHS R35 GM131763NIGMS NIH HHS R35GM131763NIH HHS S10 OD036226
6 · The paper itself

Abstract

backgroundMitochondria carry out essential functions in eukaryotic cells. The mitochondrial genome encodes factors critical to support oxidative phosphorylation and mitochondrial protein import necessary for these functions. However, organisms like budding yeast can readily lose their mitochondrial genome, yielding respiration-deficient petite mutants. The fission yeast Schizosaccharomyces pombe is petite-negative, but some nuclear mutations enable the loss of its mitochondrial genome.

resultsHere, we characterize the classical petite-positive mutation ptp1-1 as a loss of function allele of the proteasome 19S regulatory subunit component mts4/rpn1, involved in the ubiquitin-dependent degradation pathway. By comparison with another petite-enabling mutation in the g-subunit of the F

conclusionsptp1-1 is a partial loss of function mutation of the proteasome that enables growth of cells devoid of mitochondrial DNA through a mechanism that is independent of mitochondrial membrane potential rescue and associated with proteasome-dependent regulation of mitochondrial protein import precursors and the oxidative stress response.

Indexed as

Proteasome Endopeptidase ComplexSchizosaccharomycesSchizosaccharomyces pombe ProteinsMembrane Potential, MitochondrialMitochondriaMutationOxidative StressProteasome Endopeptidase ComplexSchizosaccharomyces pombe ProteinsFission yeastMitochondriaMtDNAPetiteProteasomeSchizosaccharomyces pombe

Identifiers

PMID41068765
PMCPMC12512697

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.