Jiang H et al. (2018) Viruses "The Microbial Zoo in the C. elegans Intestine: Bacteria, Fungi and Viruses."

Jiang H, Wang D

[Viruses, 2018]

<i>C. elegans</i>is an invaluable model organism that has been a driving force in many fundamental biological discoveries. However, it is only in the past two decades that it has been applied to host-pathogen interaction studies. These studies have been facilitated by the discoveries of natural microbes that infect<i>C. elegans</i>, including bacteria, fungi and viruses. Notably, many of these microbes share a common site of infection, the<i>C. elegans</i>intestine. Furthermore, the recent descriptions of a natural gut microbiota in<i>C. elegans</i>raise the possibility that this could be a novel model system for microbiome and trans-kingdom interaction studies. Here we review studies of<i>C. elegans</i>host-microbe interactions with a particular focus on the intestine.

Liu S et al. (2021) FEBS J "Multifaceted Roles of Mitochondrial Stress Responses under ETC Dysfunction - Repair, Destruction and Pathogenesis."

Liu S, Jiang H

[FEBS J, 2021]

Electron transport chain (ETC) dysfunction is a common feature of mitochondrial diseases and induces severe cellular stresses, including mitochondrial membrane potential (_m ) reduction, mitochondrial matrix acidification, metabolic derangements and proteostatic stresses. Extensive studies of ETC dysfunction in yeast, C. elegans, cultured cells and mouse models have revealed multiple mitochondrial stress response pathways. Here, we summarize the current understanding of the triggers, sensors, signaling mechanisms, and the functional outcomes of mitochondrial stress responses in different species. We highlight _m reduction as a major trigger of stress responses in different species, but the responses are species-specific and the outcomes are context-dependent. ETC dysfunction elicits a mitochondrial unfolded protein response (UPR^mt ) to repair damaged mitochondria in C. elegans, and activates a global adaptive program to maintain _m in yeast. Yeast and C. elegans responses are remarkably similar at the downstream responses, although they are activated by different signaling mechanisms. UPR^mt generally protects ETC-defective worms, but its constitutive activation is toxic for wildtype worms and worms carrying mutant mtDNA. In contrast to lower organisms, ETC dysfunction in mammals mainly activates a mitochondrial integrated stress response (ISR^mt ) to reprogram metabolism and a PINK1-Parkin mitophagy pathway to degrade damaged mitochondria. Accumulating in vivo results suggest that the ATF4 branch of ISR^mt exacerbates metabolic derangements to accelerate mitochondrial disease progression. The in vivo roles of mitophagy in mitochondrial diseases are also context-dependent. These results thus reveal the common and unique aspects of mitochondrial stress responses in different species and highlight their multifaceted roles in mitochondrial diseases.

Valles P et al. (2006) Semin Nephrol "Kidney vacuolar H+ -ATPase: physiology and regulation."

Wysocki J, Batlle D, Lapointe MS, Valles P

[Semin Nephrol, 2006]

The vacuolar H(+)-ATPase is a multisubunit protein consisting of a peripheral catalytic domain (V(1)) that binds and hydrolyzes adenosine triphosphate (ATP) and provides energy to pump H(+) through the transmembrane domain (V(0)) against a large gradient. This proton-translocating vacuolar H(+)-ATPase is present in both intracellular compartments and the plasma membrane of eukaryotic cells. Mutations in genes encoding kidney intercalated cell-specific V(0) a4 and V(1) B1 subunits of the vacuolar H(+)-ATPase cause the syndrome of distal tubular renal acidosis. This review focuses on the function, regulation, and the role of vacuolar H(+)-ATPases in renal physiology. The localization of vacuolar H(+)-ATPases in the kidney, and their role in intracellular pH (pHi) regulation, transepithelial proton transport, and acid-base homeostasis are discussed.

Kreeger KY (1996) The Scientist "Hot papers: Programmed cell death."

Kreeger KY

[The Scientist, 1996]

Biologist H. Robert Horvitz discusses the genetics of cell death in the nematode C. elegans.

Ciche T (2007) WormBook "The biology and genome of Heterorhabditis bacteriophora."

Ciche T

[WormBook, 2007]

Heterorhabditis bacteriophora is an entomopathogenic nematode (EPN) mutually associated with the enteric bacterium, Photorhabdus luminescens, used globally for the biological control of insects. Much of the previous research concerning H. bacteriophora has dealt with applied aspects related to biological control. However, H. bacteriophora is an excellent model to investigate fundamental processes such as parasitism and mutualism in addition to its comparative value to Caenorhabditis elegans. In June 2005, H. bacteriophora was targeted by NHGRI for a high quality genome sequence. This chapter summarizes the biology of H. bacteriophora in common and distinct from C. elegans, as well as the status of the genome project.

Nikolaou S et al. (2006) Int J Parasitol "Prospects for exploring molecular developmental processes in Haemonchus contortus."

Gasser RB, Nikolaou S

[Int J Parasitol, 2006]

Haemonchus contortus of small ruminants is a parasitic nematode of major socio-economic importance world-wide. While there is considerable knowledge of the morphological changes which take place during the life cycle of H. contortus, very little is understood about the molecular and biochemical processes which govern developmental changes in the parasite. Recent technological advances and the imminent genomic sequence for H. contortus provide unique opportunities to investigate the molecular basis of such processes in parasitic nematodes. This article reviews molecular and biochemical aspects of development in H. contortus, reports on some recent progress on signal transduction molecules in this parasite and emphasises the opportunities that new technologies and the free-living nematode, Caenorhabditis elegans, offer for investigating developmental aspects in H. contortus and related strongylid nematodes, also in relation to developing novel approaches for control.

Fallone CA (2000) Can J Gastroenterol "Epidemiology of the antibiotic resistance of Helicobacter pylori in Canada."

Fallone CA

[Can J Gastroenterol, 2000]

BACKGROUND: The rate of Helicobacter pylori resistance to antibiotics determines the cure rate of treatment regimens containing such antibiotics. AIMS: To review the literature to determine the rates of H pylori resistance to metronidazole and clarithromycin in Canada, and whether these rates vary in different regions of Canada. METHODS: The literature was reviewed extensively for the prevalence of antibiotic-resistant H pylori in Canada by searching MEDLINE from January 1980 to May 1999, as well as abstracts of the American Gastroenterology Association Digestive Disease Week, Canadian Digestive Disease Week and The European H pylori Study Group Meetings from January 1995 to May 1999. RESULTS: Eleven studies that estimated H pylori resistance to metronidazole resistance and nine that estimated resistance to clarithromycin in Canada were identified. Rates of resistance for metronidazole and clarithromycin varied from 11% to 48% and 0% to 12%, respectively. Studies that obtained their estimates using the E-test and those that did not clearly exclude patients who had undergone previous attempts at H pylori eradication had higher estimates of resistance, accounting for this variability in results. CONCLUSIONS: The prevalence of primary H pylori resistance in Canada appears to be 18% to 22% for metronidazole and less than 4% for clarithromycin. These rates appear to be consistent across the different regions studied in Canada, but many regions have not been studied.

Mukhopadhyay A et al. (2006) Exp Gerontol "Worming pathways to and from DAF-16/FOXO."

Tissenbaum HA, Oh SW, Mukhopadhyay A

[Exp Gerontol, 2006]

In Caenorhabditis elegans, the insulin/IGF-1 signaling pathway controls many biological processes such as life span, fat storage, dauer diapause, reproduction and stress response . This pathway is comprised of many genes including the insulin/IGF-1 receptor (DAF-2) that signals through a conserved PI 3-kinase/AKT pathway and ultimately down-regulates DAF-16, a forkhead transcription factor (FOXO). DAF-16 also receives input from several other pathways that regulate life span such as the germline and the JNK pathway [Hsin, H., Kenyon, C., 1999. Signals from the reproductive system regulate the lifespan of C. elegans. Nature 399, 362-366; Oh, S.W., Mukhopadhyay, A., Svrzikapa, N., Jiang, F., Davis, R.J., Tissenbaum, H.A., 2005. JNK regulates lifespan in Caenorhabditis elegans by modulating nuclear translocation of forkhead transcription factor/DAF-16. Proc. Natl. Acad. Sci. USA 102, 4494-4499]. Therefore, DAF-16 integrates signals from multiple pathways and regulates its downstream target genes to control diverse processes. Here, we discuss the signals to and from DAF-16, with a focus on life span regulation.

Sternberg PW et al. (1999) Nature Cell Biology "Caveolin, cholesterol and Ras signalling."

Schmid SL, Sternberg PW

[Nature Cell Biology, 1999]

Studies on the role of cholesterol- and caveolin-rich membrane microdomains in localizing Ras to the plasma membrane and enabling its signalling activity reveal intriguing differences both between mammalian H-Ras and K-Ras and between requirements for Ras signalling in mammalian and nematode cells.

Waldmann R et al. (1998) Curr Opin Neurobiol "H+-gated cation channels: nruonal acid sensors in the NaC/DEG family of ion channels."

Waldmann R, Lazdunski M

[Curr Opin Neurobiol, 1998]

Ion channels in the amiloride-sensitive Na+ channel/degenerin (NaC/DEG) family of cation channels have very diverse functions. They can be constitutively active (e.g. the epithelial Na+ channel), gated by a ligand (e.g. the peptide-gated channel FaNaC or H+-gated cation channels [ASICs]) or possibly activated by stretch (degenerins of Caenorhabditis elegans). Despite this functional diversity, the heterologous expressed channels share the following properties: permeability to Na+, inhibition by the diuretic amiloride and no voltage gating. This review will focus on recent advances in this ion channel family, with special emphasis on H+-gated cation channels.