Centriolar satellites are multiprotein aggregates that orbit the centrosome and govern centrosome homeostasis and primary cilia formation. In contrast to the scaffold PCM1, which nucleates centriolar satellites and has been linked to microtubule dynamics, autophagy, and intracellular trafficking, the functions of its interactant CEP131 beyond ciliogenesis remain unclear. Using a knockout strategy in a non-ciliary T-cell line, we report that, although dispensable for centriolar satellite assembly, CEP131 participates in optimal tubulin glycylation and polyglutamylation, and microtubule regrowth. Our unsupervised label-free proteomic analysis by quantitative mass spectrometry further uncovered mitochondrial and apoptotic signatures. CEP131-deficient cells showed an elongated mitochondrial network. Upon cell death inducers targeting mitochondria, knockout cells displayed delayed cytochrome c release from mitochondria, subsequent caspase activation, and apoptosis. This mitochondrial permeabilization defect was intrinsic, and replicable in vitro with isolated organelles. These findings extend CEP131 functions to life-and-death decisions and propose ways to interfere with mitochondrial apoptosis.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10724242 | PMC |
http://dx.doi.org/10.1038/s42003-023-05676-3 | DOI Listing |
Biogerontology
December 2024
Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, China.
Mitochondrial DNA encodes essential components of the respiratory chain complexes, serving as the foundation of mitochondrial respiratory function. Mutations in mtDNA primarily impair energy metabolism, exerting far-reaching effects on cellular physiology, particularly in the context of aging. The intrinsic vulnerability of mtDNA is increasingly recognized as a key driver in the initiation of aging and the progression of its related diseases.
View Article and Find Full Text PDFVet Sci
December 2024
Guangdong Provincial Key Laboratory of Large Animal Models for Biomedicine, South China Institute of Large Animal Models for Biomedicine, School of Pharmacy and Food Engineering, Wuyi University, Jiangmen 529000, China.
Caffeic acid phenethyl ester (CAPE) is one of the main active components of the natural medicine propolis, which has antioxidant, anti-tumor, and immunomodulatory activities. This study aimed to analyze the effects and underlying mechanisms of CAPE added to the medium of in vitro cultures on the developmental competence, mitochondria, and endoplasmic reticulum of porcine embryos. The results demonstrated that 1 nM of CAPE significantly improved the quality of porcine embryos, increased the rate of blastocyst formation, and enhanced the proliferation ability.
View Article and Find Full Text PDFMetabolites
November 2024
Research Laboratory in Applied Metabolic Engineering, Department of Chemical Engineering, Polytechnique Montréal, Centre-Ville Station, P.O. Box 6079, Montréal, QC H3C 3A7, Canada.
: This study explores the generation of singlet oxygen (SO) through methylene blue (MB) activation as a metabolic intervention for ovarian cancer. We aimed to examine the role of SO in modulating mitochondrial function, cellular metabolism, and proliferation in ovarian cancer cell lines compared to control cells. : The study utilized two ovarian cancer cell lines, OV1369-R2 and TOV1369, along with ARPE-19 control cells.
View Article and Find Full Text PDFMar Drugs
November 2024
BB21 Plus Program, Department of Chemistry, Pukyong National University, Busan 48513, Republic of Korea.
Melanoma is an aggressive skin cancer with a high risk of cancer-related deaths, and inducing apoptosis in melanoma cells is a promising therapeutic strategy. This study investigates the anti-tumor potential of a novel lucknolide derivative LA-UC as a therapeutic candidate for melanoma. Lucknolide A (LA), a tricyclic ketal-lactone metabolite isolated from marine-derived sp.
View Article and Find Full Text PDFJ Dev Biol
November 2024
Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Barth syndrome (BTHS) is a rare, infantile-onset, X-linked mitochondriopathy exhibiting a variable presentation of failure to thrive, growth insufficiency, skeletal myopathy, neutropenia, and heart anomalies due to mitochondrial dysfunction secondary to inherited TAFAZZIN transacetylase mutations. Although not reported in BTHS patients, male infertility is observed in several () mouse alleles and in a mutant. Herein, we examined the male infertility phenotype in a BTHS-patient-derived point-mutant knockin mouse () allele that expresses a mutant protein lacking transacetylase activity.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!