Verma A et al. (2016) Int J Biol Macromol "NADP(+) binding effects tryptophan accessibility, folding and stability of recombinant B. malayi G6PD."

Verma A, Siddiqi MI, Suthar MK, Chandra S, Saxena JK, Doharey PK

[Int J Biol Macromol, 2016]

Brugia malayi Glucose 6-phosphate dehydrogenase apoenzyme (BmG6PD) was expressed and purified by affinity chromatography to study the differences in kinetic properties of enzyme and the effect of the cofactor NADP(+) binding on enzyme stability. The presence of cofactor NADP(+) influenced the tertiary structure of enzyme due to significant differences in the tryptophan microenvironment. However, NADP(+) binding have no effect on secondary structure of the enzyme. Quenching with acrylamide indicated that two or more tryptophan residues became accessible upon cofactor binding. Unfolding and cross linking study of BmG6PD showed that NADP(+) stabilized the protein in presence of high concentration of urea/GdmCl. A homology model of BmG6PD constructed using human G6PD (PDB id: 2BH9) as a template indicated 34% -helix, 19% -sheet and 47% random coil conformations in the predicted model of the enzyme. In the predicted model binding of NADP(+) to BmG6PD was less tight with the structural sites (-10.96 KJ/Mol binding score) as compared with the coenzyme site (-15.47 KJ/Mol binding score).

Nicholas WL et al. (1978) Nematologica "The calorific value of C. elegans (Rhabditidae)."

Stewart AC, Nicholas WL

[Nematologica, 1978]

The calorific value of populations of Caenorhabditis elegans was measured by bomb-calorimetry. A value of 27.59 kJ per g ash-free dry weight was obtained (=6,316 calories per g). This value is high, but agrees well with calculations based on previously published analyses of lipid and glycogen reserves in Caenorhabditis sp. It is suggested that when harvested from a rich culture of bacteria Caenorhabditis has substantial lipid reserves accounting for its high calorific value.

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.

Krishna NR et al. (2013) J Enzyme Inhib Med Chem "Physicochemical characterization of an aspin (rBm-33) from a filarial parasite Brugia malayi against the important human aspartic proteases."

Krishna NR, Gunasekaran K, Krushna NS, Rajan SS, Narayanan RB

[J Enzyme Inhib Med Chem, 2013]

The aspartic protease inhibitory efficiency of rBm-33, an aspin from a filarial parasite Brugia malayi was investigated. rBm-33 was found to be thermostable up to 90C and it forms a stable 'enzyme-product' complex with human pepsin. Aspartic protease inhibitory activity was investigated using UV spectroscopy and isothermal titration calorimetry. Our results suggest that rBm-33 inhibits the activity of important human aspartic proteases that were examined with binding constants (Kb) values between 10.23 x 10(3) and 6.52 x 10(3) M(-1). The binding reactions were enthalpy driven with Hb values between -50.99 and -46.07 kJ mol(-1). From kinetic studies, pepsin inhibition by rBm-33 was found to be linear competitive with an inhibition constant (Ki) of 2.5 (+/-0.8) nM. Because of the inhibitory efficacy of Bm-33 against important human aspartic proteases which play a vital role in immune-regulation along with other functions, Bm-33 can be projected as a drug target for the filariasis.

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.