AI Article Synopsis

  • The protist Monocercomonoides exilis demonstrates that mitochondria are not essential for eukaryotic cells, prompting investigation into its genomic adaptations.
  • The genome of M. exilis has a complexity comparable to other eukaryotes, and its cellular structures display canonical eukaryotic traits despite lacking mitochondria.
  • The study suggests that the loss of mitochondria is accompanied by adaptations in metabolism and stress response, positioning M. exilis as a valuable model for eukaryotic cell biology research without mitochondria.

Article Abstract

The discovery that the protist Monocercomonoides exilis completely lacks mitochondria demonstrates that these organelles are not absolutely essential to eukaryotic cells. However, the degree to which the metabolism and cellular systems of this organism have adapted to the loss of mitochondria is unknown. Here, we report an extensive analysis of the M. exilis genome to address this question. Unexpectedly, we find that M. exilis genome structure and content is similar in complexity to other eukaryotes and less "reduced" than genomes of some other protists from the Metamonada group to which it belongs. Furthermore, the predicted cytoskeletal systems, the organization of endomembrane systems, and biosynthetic pathways also display canonical eukaryotic complexity. The only apparent preadaptation that permitted the loss of mitochondria was the acquisition of the SUF system for Fe-S cluster assembly and the loss of glycine cleavage system. Changes in other systems, including in amino acid metabolism and oxidative stress response, were coincident with the loss of mitochondria but are likely adaptations to the microaerophilic and endobiotic niche rather than the mitochondrial loss per se. Apart from the lack of mitochondria and peroxisomes, we show that M. exilis is a fully elaborated eukaryotic cell that is a promising model system in which eukaryotic cell biology can be investigated in the absence of mitochondria.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6759080PMC
http://dx.doi.org/10.1093/molbev/msz147DOI Listing

Publication Analysis

Top Keywords

loss mitochondria
12
canonical eukaryotic
8
eukaryotic complexity
8
exilis genome
8
eukaryotic cell
8
mitochondria
6
eukaryotic
5
loss
5
oxymonad genome
4
genome displays
4

Similar Publications

Viruses are dependent on cellular energy metabolism for their replication, and the drug nitazoxanide (Alinia) was shown to interfere with both processes. Nitazoxanide is an uncoupler of mitochondrial oxidative phosphorylation (OXPHOS). Our hypothesis was that mitochondrial uncoupling underlies the antiviral effects of nitazoxanide.

View Article and Find Full Text PDF

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 PDF

The Vsr-like protein FASTKD4 regulates the stability and polyadenylation of the MT-ND3 mRNA.

Nucleic Acids Res

December 2024

The Kids Research Institute Australia, Northern Entrance, Perth Children's Hospital, 15 Hospital Avenue, Nedlands, Western Australia 6009, Australia.

Expression of the compact mitochondrial genome is regulated by nuclear encoded, mitochondrially localized RNA-binding proteins (RBPs). RBPs regulate the lifecycles of mitochondrial RNAs from transcription to degradation by mediating RNA processing, maturation, stability and translation. The Fas-activated serine/threonine kinase (FASTK) family of RBPs has been shown to regulate and fine-tune discrete aspects of mitochondrial gene expression.

View Article and Find Full Text PDF

Dysfunctional copper homeostasis in affects genomic and neuronal stability.

Redox Biochem Chem

December 2024

Food Chemistry with Focus on Toxicology, Faculty of Mathematics and Natural Sciences, University of Wuppertal, Germany.

While copper (Cu) is an essential trace element for biological systems due to its redox properties, excess levels may lead to adverse effects partly due to overproduction of reactive species. Thus, a tightly regulated Cu homeostasis is crucial for health. Cu dyshomeostasis and elevated labile Cu levels are associated with oxidative stress and neurodegenerative disorders, but the underlying mechanisms have yet to be fully characterized.

View Article and Find Full Text PDF

Background: Inclusion body myositis (IBM) is the most prevalent muscle disease in adults for which no current treatment exists. The pathogenesis of IBM remains poorly defined. In this study, we aimed to explore the interplay between inflammation and mitochondrial dysfunction in IBM.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!