Caenorhabditis elegans pathways that surveil and defend mitochondria

Liu, Ying; Samuel, Buck S.; Breen, Peter C.; Ruvkun, Gary

doi:10.1038/nature13204

Cited by 265 publications

(334 citation statements)

References 24 publications

(29 reference statements)

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“…Interestingly, a mutant of the mitochondrial division protein DRP3A, with a chondriome comprising elongated and interconnected mitochondrial tubules, was identified in the same screen, suggesting that chondriome structure per se is important for plant defense responses to pathogens. Taken together, the disruption of mitochondrial chondriome structure in response to biotic and abiotic stress (Gao et al, 2008;Scott and Logan, 2008;Zhang and Xing, 2008), the reduced ability of plants with altered chondriome structure to fight pathogen attack (Vellosillo et al, 2013), and the stress phenotypes in the friendly mutant (this work) suggest that in plants, as in animals (Runkel et al, 2013;Liu et al, 2014), mitochondria perform the role of sentinels whereby disruption of mitochondrial function is interpreted as an attack on the cell and that chondriome structure is important for the defense response.…”

Section: Discussionmentioning

confidence: 99%

FRIENDLY Regulates Mitochondrial Distribution, Fusion, and Quality Control in Arabidopsis

et al. 2014

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Mitochondria are defining components of most eukaryotes. However, higher plant mitochondria differ biochemically, morphologically, and dynamically from those in other eukaryotes. FRIENDLY, a member of the CLUSTERED MITOCHONDRIA superfamily, is conserved among eukaryotes and is required for correct distribution of mitochondria within the cell. We sought to understand how disruption of FRIENDLY function in Arabidopsis (Arabidopsis thaliana) leads to mitochondrial clustering and the effects of this aberrant chondriome on cell and whole-plant physiology. We present evidence for a role of FRIENDLY in mediating intermitochondrial association, which is a necessary prelude to mitochondrial fusion. We demonstrate that disruption of mitochondrial association, motility, and chondriome structure in friendly affects mitochondrial quality control and leads to mitochondrial stress, cell death, and strong growth phenotypes.

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Section: Discussionmentioning

confidence: 99%

FRIENDLY Regulates Mitochondrial Distribution, Fusion, and Quality Control in Arabidopsis

et al. 2014

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“…elegans was grown on each individual cultivated bacterial strain from our collection (565 isolates included), and we assayed rates of growth and induction of stress and immune reporter genes (Dataset S3). These reporters were chosen to monitor whether C. elegans may respond to any of the bacterial species as a pathogenic stress (24)(25)(26)(27). We expected that natural pathogens or competitors isolated from the rotting fruit would induce expression of these stress or immunity reporter genes, whereas relatively benign or even beneficial bacteria would not.…”

Section: Resultsmentioning

confidence: 99%

“…S3), suggesting that toxin concentrations may not have reached appropriate thresholds for activation or that there are widespread programs for active suppression of the worm's response by bacteria (as was shown for natural Pseudomonas spp. suppression of hsp-6::GFP activation following mitochondrial stress) (25).…”

Section: Resultsmentioning

confidence: 99%

Caenorhabditis elegans responses to bacteria from its natural habitats

Samuel

Rowedder

Braendle

et al. 2016

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

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316

412

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Most Caenorhabditis elegans studies have used laboratory Escherichia coli as diet and microbial environment. Here we characterize bacteria of C. elegans' natural habitats of rotting fruits and vegetation to provide greater context for its physiological responses. By the use of 16S ribosomal DNA (rDNA)-based sequencing, we identified a large variety of bacteria in C. elegans habitats, with phyla Proteobacteria, Bacteroidetes, Firmicutes, and Actinobacteria being most abundant. From laboratory assays using isolated natural bacteria, C. elegans is able to forage on most bacteria (robust growth on ∼80% of >550 isolates), although ∼20% also impaired growth and arrested and/or stressed animals. Bacterial community composition can predict wild C. elegans population states in both rotting apples and reconstructed microbiomes: alpha-Proteobacteria-rich communities promote proliferation, whereas Bacteroidetes or pathogens correlate with nonproliferating dauers. Combinatorial mixtures of detrimental and beneficial bacteria indicate that bacterial influence is not simply nutritional. Together, these studies provide a foundation for interrogating how bacteria naturally influence C. elegans physiology.Caenorhabditis elegans | host-microbe interactions | ecology B iological organisms constantly live in contact with other organisms in a complex web of ecological interactions, which include prey-predator, host-parasite, competitive, or positive symbiotic relationships. Bacteria are now considered key players in multiple aspects of the biology of multicellular organisms (1-3). The richness and importance of these interactions were so far neglected because laboratory biology had succeeded in simplifying and standardizing the environment of the model organisms, providing in most cases a single microbe as a food source, and not necessarily even a naturally encountered one. The many aspects of organismal biology that were shaped by evolution in natural environments are thus undetectable in the artificial laboratory environment and can only be revealed in the presence of other interacting species. Examples include feeding behavior, metabolism of diverse natural food sources, interactions with natural pathogens that have shaped the organism's immune system, behavioral traits, and regulation of development and reproduction. At the genomic level, many individual genes may not be required in a standard laboratory environment but their role may be revealed by using more diverse and relevant environments (4, 5).The nematode Caenorhabditis elegans is a typical example of a model organism that has been disconnected from its natural ecology: although the species has been studied intensively in the laboratory for half a century, its habitat and natural ecology-what it naturally feeds on, its natural predators and pathogens,

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“…Using a genetic approach, two metabolic pathways were identified as important regulators of the UPR mt (18). First, knockdown of components in the sphingolipid biosynthesis pathway, including the enzymes serine palmitoyltransferase and ceramide synthase, results in UPR mt attenuation that can be rescued with ceramide supplementation.…”

Section: Caenorhabditis Elegansmentioning

confidence: 99%

The mitochondrial unfolded protein response: Signaling from the powerhouse

Qureshi

Haynes

Pellegrino

2017

Journal of Biological Chemistry

122

109

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Edited by Ruma BanerjeeMitochondria are multifaceted and indispensable organelles required for cell performance. Accordingly, dysfunction to mitochondria can result in cellular decline and possibly the onset of disease. Cells use a variety of means to recover mitochondria and restore homeostasis, including the activation of retrograde pathways such as the mitochondrial unfolded protein response (UPR mt ). In this Minireview, we will discuss how cells adapt to mitochondrial stress through UPR mt regulation. Furthermore, we will explore the current repertoire of biological functions that are associated with this essential stress-response pathway.Mitochondria are double membrane organelles commonly associated with the production of cellular energy via oxidative phosphorylation (OXPHOS).2 Mitochondria are also required for the metabolism of nucleotides, amino acids, and lipids and have an essential function in regulating apoptosis. Maintaining mitochondrial integrity is therefore a key aspect in ensuring cellular and organismal viability. Consequently, a decline in mitochondrial function is frequently associated with the development of numerous diseases (1).Mitochondria are dependent on a diverse compilation of proteins to carry out their vital functions. However, the mitochondrial proteome is faced with various challenges, most notably the partitioning of protein encoding genes between the mitochondrial and nuclear genomes. Remarkably, the human mitochondrial genome only encodes ϳ1% of the total mitochondrial proteome with the remaining proteins being encoded by nuclear genes (2). Sophisticated mechanisms have evolved to efficiently transfer nuclear-encoded mitochondrial proteins to their proper organelle destination following translation on cytosolic ribosomes. To accomplish this complex task, proteins are sorted to mitochondria via targeting sequences that form characteristic amphipathic helices composed of positively charged residues. Such mitochondrial targeting sequences (MTS) are recognized and translocated via the mitochondrial Tom-Tim complex to their respective sub-organelle compartment (3). Exquisite coordination of expression between the mitochondrial and nuclear genomes exists during mitochondrial biogenesis, as failure in genome coordination can disrupt the precise stoichiometry of these OXPHOS complexes resulting in orphan subunit accumulation and proteotoxicity (4). Further contributing to mitochondrial proteotoxicity is the possible damage to the mitochondrial genome from reactive oxygen species (ROS) produced by OXPHOS machinery as well as the ill effects of various environmental toxins. Mechanisms must therefore exist to ensure the protection of the mitochondrial proteome.Quality control of the mitochondrial proteome includes the functions of mitochondrial chaperones that assist in proper protein folding and proteases that promote clearance of misfolded proteins (5). Each sub-compartment of mitochondria houses its own quality control machinery to ensure protein homeostasis and organelle function. ...

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Caenorhabditis elegans pathways that surveil and defend mitochondria

Cited by 265 publications

References 24 publications

FRIENDLY Regulates Mitochondrial Distribution, Fusion, and Quality Control in Arabidopsis

FRIENDLY Regulates Mitochondrial Distribution, Fusion, and Quality Control in Arabidopsis

Caenorhabditis elegans responses to bacteria from its natural habitats

The mitochondrial unfolded protein response: Signaling from the powerhouse

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