Presentation Title

Characterizing the Function of UBC-1 in the Neurons of C. elegans

Start Date

November 2016

End Date

November 2016

Location

HUB 302-#134

Type of Presentation

Poster

Abstract

E2 ubiquitin-conjugating enzymes interact with E3 ubiquitin ligase to covalently attach a chain of ubiquitin to a lysine residue on a substrate. This targets the marked substrate for proteasomal degradation. A mutation to the human Rad6a (Ube2a) gene encodes for a defective E2 enzyme that has been discovered in patients with X-linked intellectual disabilities (Haddad et al., Mol. Cell 2013). The homolog in C. elegans is the E2 ubiquitin-conjugating enzyme UBC-1, but the function of UBC-1 in the nervous system of C. elegans is unknown. However, C. elegans with ubc-1 mutants display poor health as they are uncoordinated, have low brood size, and suffer from synaptic defects. The mutation can be partially rescued through expressing UBC-1 in neurons or intestinal cells. To determine the cellular and sub-cellular expression of UBC-1 in C. elegans, two transgenes, PSU006 GFP UBC-1 and PUNC-25 GFP UBC-1, were constructed using restriction digest techniques. PSU006 is a pan neuronal promoter, while PUNC-25 is a GABAergic neuron promoter. The two constructs were completed and successfully expressed in bacteria. Injections into C. elegans to create transgenic worms are in process. The information found through this research will be helpful in characterizing the effects of this mutation in C. elegans, and may lead to a better understanding the human Rad6a (Ube2a) gene and its correlation with X-linked intellectual disabilities.

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Characterizing the Function of UBC-1 in the Neurons of C. elegans

HUB 302-#134

E2 ubiquitin-conjugating enzymes interact with E3 ubiquitin ligase to covalently attach a chain of ubiquitin to a lysine residue on a substrate. This targets the marked substrate for proteasomal degradation. A mutation to the human Rad6a (Ube2a) gene encodes for a defective E2 enzyme that has been discovered in patients with X-linked intellectual disabilities (Haddad et al., Mol. Cell 2013). The homolog in C. elegans is the E2 ubiquitin-conjugating enzyme UBC-1, but the function of UBC-1 in the nervous system of C. elegans is unknown. However, C. elegans with ubc-1 mutants display poor health as they are uncoordinated, have low brood size, and suffer from synaptic defects. The mutation can be partially rescued through expressing UBC-1 in neurons or intestinal cells. To determine the cellular and sub-cellular expression of UBC-1 in C. elegans, two transgenes, PSU006 GFP UBC-1 and PUNC-25 GFP UBC-1, were constructed using restriction digest techniques. PSU006 is a pan neuronal promoter, while PUNC-25 is a GABAergic neuron promoter. The two constructs were completed and successfully expressed in bacteria. Injections into C. elegans to create transgenic worms are in process. The information found through this research will be helpful in characterizing the effects of this mutation in C. elegans, and may lead to a better understanding the human Rad6a (Ube2a) gene and its correlation with X-linked intellectual disabilities.