C. elegans

Abstract

To gain insights into the genetic cascades that regulate fat biology, we evaluated C. elegans as an appropriate model organism. We generated worms that lack two transcription factors, SREBP and C/EBP, crucial for formation of mammalian fat. Worms deficient in either of these genes displayed a lipid-depleted phenotype-pale, skinny, larval-arrested worms that lack fat stores. On the basis of this phenotype, we used a reverse genetic screen to identify several additional genes that play a role in worm lipid storage. Two of the genes encode components of the mitochondrial respiratory chain (MRC). When the MRC was inhibited chemically in worms or in a mammalian adipocyte model, fat accumulation was markedly reduced. A third encodes lpd-3, whose homolog is also required for fat storage in a mammalian model. These data suggest that C. elegans is a genetically tractable model to study the mechanisms that underlie the biology of fat-storing tissues.

Mitochondrial Reactive Oxygen Species Control the Transcription Factor CHOP-10/GADD153 and Adipocyte Differentiation

“…Thus, the concept that mitochondria could play an essential role in white adipose tissue development is now emerging. This is consistent with another study, which reports that genes encoding components of the mitochondrial respiratory chain play an essential role in lipid storage (7). Beside their key role in ATP production, mitochondria constitute the primary source of reactive oxygen species (ROS) generation in many cells.…”

The African turquoise killifish: A research organism to study vertebrate aging and diapause

“…(b) Selected features of the turquoise killifish that are conserved in human and vertebrate canonical research organisms (zebrafish and house mouse), but are missing in invertebrate canonical research organisms (round worm and fruit fly). References: nervous system: Shimeld and Holland (2000), Freeman and Doherty (2006); Lohr and Hammerschmidt (2011), Oikonomou and Shaham (2011), immune system: Langenau and Zon (2005), Engelmann and Pujol (2010), Buchon, Silverman and Cherry ( 2014); circulatory system: Lehmacher, Abeln and Paululat ( 2012); Stephenson, Adams and Vaccarezza ( 2017); respiratory system: Schottenfeld, Song and Ghabrial ( 2010); skeletal system: Shimeld and Holland (2000); muscular system: Moerman and Williams (2006), Demontis, Piccirillo, Goldberg and Perrimon ( 2013), Piccirillo, Demontis, Perrimon and Goldberg ( 2014), Goody, Carter, Kilroy, Maves and Henry ( 2017); digestive system: McKay, McKay, Avery and Graff ( 2003), Arrese and Soulages (2010), Hashmi et al. ( 2013), Kuraishi, Hori and Kurata ( 2013), Lemaitre and Miguel‐Aliaga (2013), McGhee (2013), Ritter et al.…”

Caenorhabditis elegans UCP4 Protein Controls Complex II-mediated Oxidative Phosphorylation through Succinate Transport

“…The nematode C. elegans is a powerful model for understanding mechanisms regulating mammalian energy homeostasis because the vast majority of metabolic genes are conserved (8,9). Unlike most other organisms, C. elegans expresses only a single UCP ortholog, ceUCP4, which shares 46% homology (amino acid) with human UCP4 (5).…”