Elucidating determinants at the Gšœ¶13 N-terminus for binding to the šœ·šœø dimer

Monday, November 25, 12:50pm – 1:10pm, Zeis 123, via Zoom

Forbes Fowler

Dr. Ted Meigs

Heterotrimeric guanine nucleotide-binding proteins (G proteins)

are cell signaling conduits composed of the subunits š›¼, š›½, and š›¾.

These proteins relay signals from cell surface receptors to various

downstream effector proteins. The š›¼ subunits Gš›¼12 and Gš›¼13 are

implicated in multiple tumor types as wildtype (WT) and

constitutively active (QL) forms. Gš›¼13 is overexpressed in

multiple tumor types including invasive breast cancer, prostate

adenocarcinoma, and ovarian cystadenocarcinoma. It is crucial to

identify potential therapeutic sites in Gš›¼13, and considerable work

has examined its mechanism of binding to downstream effectors as

well as its post-translational modifications. No studies have

precisely defined the amino acids of Gš›¼13 required for binding the

š›½š›¾ dimer, nor whether initial association with š›½š›¾ is necessary for

lipid modifications of Gš›¼13. We have sought to identify amino

acids in Gš›¼13 required for binding to the š›½ subunit, and also

determine whether association with š›½š›¾ is necessary for signaling

by Gš›¼13WT compared to the QL form. Therefore, we mutated

amino acids in Gš›¼13 previously suggested as N-terminal contact

points with the š›½ subunit. Also, recent work by Wedegaertner and

colleagues identified a single amino acid within a different G

subunit, Gš›¼q, that is crucial for its binding to š›½ (Aumiller and

Wedegaertner 2023). Based on Gš›¼q and Gš›¼13 alignment, we also

engineered a single amino acid mutation in Gš›¼13 WT and QL. All

mutants were expressed in HEK293 cells, and lysates were used in

a glutathione-S-transferase (GST) pulldown assay. Precipitates

were subjected to immunoblotting to determine the presence of

Gš›¼13 variants in the sepharose-bound š›½ subunit samples.

Preliminary results suggest these mutations disrupt both Gš›¼13 WT

and QL binding to the š›½ subunit. Currently we are examining these

mutants for tumorigenic growth signaling and ability to interact

with other known binding partners of Gš›¼13.