The Role of Lin-46, Moc-1, and Molybdenum Cofactor in C. Elegans Development

Overview

Molybdenum is an essential trace element. In biological systems it exists as Molybdenum Cofactor (MoCo), the synthesis of which is performed by Gephyrin. Mutations in human Gephyrin lead to MoCo deficiency, which generally cause death within the first week of life. The Gephyrin genes are evolutionarily conserved from humans to bacteria. Two genes in C. elegans, Lin-46 and Moc-1, share sequence homology to bacterial (MoeA) and mammalian Gephyrin. Mutations in Lin-46 in particular were further found to be involved in embryonic development, but the mechanism was unclear. Using a strain of E. coli deficient in MoCo (a MoeA deletion) to control for nutritional provision of Molybdenum Cofactor, I conducted growth assays of worms mutated in either the Lin-46 or Moc-1 genes. I then constructed a C. elegans strain mutated for both genes, and conducted a growth assay. All three strains of C. elegans were found to have reduced growth when consuming MoCo-deficient bacteria. This defect was most pronounced in the Moc-1 mutant and the Moc-1:Lin-46 double mutant. However, those two strains also had far less growth than control and Lin-46 mutated strains on MoCo sufficient bacteria, suggesting that the mutations affected processes independent of MoCo synthesis.

Competition history

• AJAS 2017 Category not listed

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