(2019) Development "The people behind the papers - Julia Brandt, Mary Rossillo and Niels Ringstad."

[Development, 2019]

A fundamental aim in developmental biology is to understand how the various cell types of the body are specified by differential gene regulation. <i>Caenorhabditis</i><i>elegans</i> nervous system development provides a powerful system for studying this, as exemplified by a new Development paper reporting on how the BAG neurons that help the worm sense oxygen and carbon dioxide are specified. We caught up with first authors Julia Brandt and Mary Rossillo and their supervisor Niels Ringstad (Associate Professor at the Skirball Institute of Biomolecular Medicine and Department of Cell Biology at New York University) to find out more about the story.

Deng H et al. (2021) Proc Natl Acad Sci U S A "SLC-30A9 is required for Zn2+ homeostasis, Zn2+ mobilization, and mitochondrial health."

Deng H, Feng Y, Li H, Guo M, Chen C, Zhao Y, Xie T, Fu W, Miao L, Chen L, Qiao X, Shen K, Wang X

[Proc Natl Acad Sci U S A, 2021]

The trace element zinc is essential for many aspects of physiology. The mitochondrion is a major Zn2+ store, and excessive mitochondrial Zn2+ is linked to neurodegeneration. How mitochondria maintain their Zn2+ homeostasis is unknown. Here, we find that the SLC-30A9 transporter localizes on mitochondria and is required for export of Zn2+ from mitochondria in both Caenorhabditis elegans and human cells. Loss of slc-30a9 leads to elevated Zn2+ levels in mitochondria, a severely swollen mitochondrial matrix in many tissues, compromised mitochondrial metabolic function, reductive stress, and induction of the mitochondrial stress response. SLC-30A9 is also essential for organismal fertility and sperm activation in C. elegans, during which Zn2+ exits from mitochondria and acts as an activation signal. In slc-30a9-deficient neurons, misshapen mitochondria show reduced distribution in axons and dendrites, providing a potential mechanism for the Birk-Landau-Perez cerebrorenal syndrome where an SLC30A9 mutation was found.

Dasgupta, Madhumanti et al. (2020) MicroPubl Biol

Singh, Varsha, Shashikanth, Meghana, Dasgupta, Madhumanti, Bojanala, Nagagireesh

[MicroPubl Biol, 2020]

Caenorhabditis elegans feeds on bacteria in decomposing vegetation. Lipids, carbohydrates and proteins derived from microbes are digested into fatty acids, simple sugars and amino acids in C. elegans alimentary canal and absorbed by intestinal cells containing microvilli. Approximately 80% of fatty acids in C. elegans is derived from E. coli (Perez and Van Gilst, 2008). Nutrient limiting conditions can cause developmental delay in larvae (Cassada and Russell, 1975; Golden and Riddle, 1982) while complete starvation leads to L1 larval arrest or dauer formation (Baugh, 2013). Interestingly it has been reported that C. elegans fed on yeast Cryptococcus curvatus show developmental lag (Sanghvi et al., 2016) and growth arrest on Gram-positive bacterium Enterococcus faecalis (Garsin et al., 2001). We have recently shown that E. faecalis infection causes lipid droplet utilization in adult C. elegans, a process termed immunometabolism (Dasgupta et al., 2020). In this study, we have investigated the developmental arrest induced by E. faecalis in C. elegans larvae to show that the arrest is induced at L1 and L2 larva stage.