Lipid and carbohydrate metabolism are highly conserved processes that affect nearly all aspects of organismal biology. Caenorhabditis elegans eat bacteria, which consist of lipids, carbohydrates, and proteins that are broken down during digestion into fatty acids, simple sugars, and amino acid precursors. With these nutrients, C. elegans synthesizes a wide range of metabolites that are required for development and behavior. In this review, we outline lipid and carbohydrate structures as well as biosynthesis and breakdown pathways that have been characterized in C. elegans We bring attention to functional studies using mutant strains that reveal physiological roles for specific lipids and carbohydrates during development, aging, and adaptation to changing environmental conditions.

https://www.genetics.org/content/genetics/207/2/413.full.pdf

Lipid and Carbohydrate Metabolism in Caenorhabditis Elegans

The Target of Rapamycin (TOR or mTOR) is a serine/threonine kinase that regulates growth, development, and behaviors by modulating protein synthesis, autophagy, and multiple other cellular processes in response to changes in nutrients and other cues. Over recent years, TOR has been studied intensively in mammalian cell culture and genetic systems because of its importance in growth, metabolism, cancer, and aging. Through its advantages for unbiased, and high-throughput, genetic and in vivo studies, Caenorhabditis elegans has made major contributions to our understanding of TOR biology. Genetic analyses in the worm have revealed unexpected aspects of TOR functions and regulation, and have the potential to further expand our understanding of how growth and metabolic regulation influence development. In the aging field, C. elegans has played a leading role in revealing the promise of TOR inhibition as a strategy for extending life span, and identifying mechanisms that function upstream and downstream of TOR to influence aging. Here, we review the state of the TOR field in C. elegans, and focus on what we have learned about its functions in development, metabolism, and aging. We discuss knowledge gaps, including the potential pitfalls in translating findings back and forth across organisms, but also describe how TOR is important for C. elegans biology, and how C. elegans work has developed paradigms of great importance for the broader TOR field.

https://www.genetics.org/content/genetics/213/2/329.full.pdf

TOR Signaling in Caenorhabditis elegans Development, Metabolism, and Aging.

Vitellogenins are a family of yolk proteins that are by far the most abundant among oviparous animals. In the model nematode Caenorhabditis elegans, the 6 vitellogenins are among the most highly expressed genes in the adult hermaphrodite intestine, which produces copious yolk to provision eggs. In this article we review what is known about the vitellogenin genes and proteins in C. elegans, in comparison with vitellogenins in other taxa. We argue that the primary purpose of abundant vitellogenesis in C. elegans is to support post-embryonic development and fertility, rather than embryogenesis, especially in harsh environments. Increasing vitellogenin provisioning underlies several post-embryonic phenotypic alterations associated with advancing maternal age, demonstrating that vitellogenins can act as an intergenerational signal mediating the influence of parental physiology on progeny. We also review what is known about vitellogenin regulation - how tissue-, sex- and stage-specificity of expression is achieved, how vitellogenins are regulated by major signaling pathways, how vitellogenin expression is affected by extra-intestinal tissues and how environmental experience affects vitellogenesis. Lastly, we speculate whether C. elegans vitellogenins may play other roles in worm physiology.

/pdf/vitellogenins-yolk-gene-function-and-regulation-in-1v4fvgl6vg.pdf

Vitellogenins - Yolk Gene Function and Regulation in Caenorhabditis elegans.

MicroRNAs are small, noncoding RNAs that regulate gene expression at the post-transcriptional level in essentially all aspects of Caenorhabditis elegans biology. More than 140 genes that encode microRNAs in C. elegans regulate development, behavior, metabolism, and responses to physiological and environmental changes. Genetic analysis of C. elegans microRNA genes continues to enhance our fundamental understanding of how microRNAs are integrated into broader gene regulatory networks to control diverse biological processes, including growth, cell division, cell fate determination, behavior, longevity, and stress responses. As many of these microRNA sequences and the related processing machinery are conserved over nearly a billion years of animal phylogeny, the assignment of their functions via worm genetics may inform the functions of their orthologs in other animals, including humans. In vivo investigations are especially important for microRNAs because in silico extrapolation of their functions using mRNA target prediction programs can easily assign microRNAs to incorrect genetic pathways. At this mezzanine level of microRNA bioinformatic sophistication, genetic analysis continues to be the gold standard for pathway assignments.

https://www.genetics.org/content/genetics/209/3/651.full.pdf

Recent Molecular Genetic Explorations of Caenorhabditis elegans MicroRNAs.

Natural genetic variation drives microbiome selection in the Caenorhabditis elegans gut.

Animals integrate metabolic, developmental, and environmental information before committing key resources to reproduction. In Caenorhabditis elegans, adult animals transport fat from intestinal cells to the germline to promote reproduction. We identified a microRNA (miRNA)-regulated developmental timing pathway that functions in the hypodermis to nonautonomously coordinate the mobilization of intestinal fat stores to the germline upon initiation of adulthood. This developmental timing pathway, which is controlled by the lin-4 and let-7 miRNAs, engages mTOR signaling in the intestine. The intestinal signaling component is specific to mTORC2 and functions in parallel to the insulin pathway to modulate the activity of the serum/glucocorticoid-regulated kinase (SGK-1). Surprisingly, SGK-1 functions independently of DAF-16/FoxO; instead, SGK-1 promotes the cytoplasmic localization of the PQM-1 transcription factor, which antagonizes intestinal fat mobilization at the transcriptional level when localized to the nucleus. These results revealed that a non-cell-autonomous developmental input regulates intestinal fat metabolism by engaging mTORC2 signaling to promote the intertissue transport of fat reserves from the soma to the germline.

/pdf/a-microrna-program-in-the-c-elegans-hypodermis-couples-to-3uninbilj4.pdf

A microRNA program in the C. elegans hypodermis couples to intestinal mTORC2/PQM-1 signaling to modulate fat transport.

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A microRNA program in the C. elegans hypodermis couples to intestinal mTORC2/PQM-1 signaling to modulate fat transport.