Disease relevance of gig

• gigas, a Drosophila homolog of tuberous sclerosis gene product-2, regulates the cell cycle [1].
• Germline mutations in either TSC1 or TSC2 cause this syndrome, and hamartomas typically display second hit events with loss of the remaining normal allele [2].
• The crystal structure of the aldehyde oxido-reductase (Mop) from the sulfate reducing anaerobic Gram-negative bacterium Desulfovibrio gigas has been determined at 2.25 A resolution by multiple isomorphous replacement and refined [3].
• Promoters from Drosophila heat shock protein and cytomegalovirus drive transient expression of luciferase introduced by particle bombardment into embryos of the oyster Crassostrea gigas [4].

Psychiatry related information on gig

• An expressed sequence tag program was undertaken to isolate genes involved in defense mechanisms of the Pacific oyster, Crassostrea gigas [5].

High impact information on gig

• We have characterized mutations in the Drosophila Tsc1 and Tsc2/gigas genes [6].
• Coexpression of both Tsc1 and Tsc2 restricts tissue growth and reduces cell size and cell proliferation [6].
• Overexpression of Tsc1 or Tsc2 alone in the wing and eye has no effect, but co-overexpression leads to a decrease in cell size, cell number, and organ size [7].
• Genetic epistasis data are consistent with a model that Tsc1 and Tsc2 function together in the insulin signaling pathway [7].
• Crystal structure of the xanthine oxidase-related aldehyde oxido-reductase from D. gigas [3].

Biological context of gig

• Drosophila Tsc1 functions with Tsc2 to antagonize insulin signaling in regulating cell growth, cell proliferation, and organ size [7].
• Tuberous sclerosis complex (TSC) is a genetic disorder caused by mutations in one of two tumor suppressor genes, TSC1 and TSC2 [8].
• Here we evaluate this model genetically in Drosophila by engineering Tsc2 mutants in which the Akt phosphorylation sites are changed to nonphosphorylatable or phospho-mimicking residues [9].
• Previous studies of a Drosophila TSC2 homolog suggested a role for the TSC genes in maintaining DNA content, with loss of TSC2 leading to polyploidy and increased cell size [10].
• Unlike previous studies, our work shows that TSC1(-) or TSC2(-) cells are diploid [10].

Anatomical context of gig

• The mutant axon does terminate its growth eventually, and the new additional targets that are reached correspond to mechanoreceptor domains in other ganglia, indicating that this territorial constraint is operational in the mutant. gigas neurons maintain their stereotyped profile and represent an expanded version of the normal branching pattern [11].
• Immune gene discovery by expressed sequence tags generated from hemocytes of the bacteria-challenged oyster, Crassostrea gigas [5].
• This confirms the suitability of particle bombardment for transfecting genes into eggs, zygotes and trochopores of bivalves and demonstrates the functionality of two heterologous expression vectors in C. gigas [4].

Associations of gig with chemical compounds

• In support of tuberin acting as a tumor suppressor, ectopic overexpression of TSC2 has been shown to decrease proliferation rates of mammalian cells [12].

Other interactions of gig

• Tsc2 is not a critical target of Akt during normal Drosophila development [9].
• We report here the identification and functional characterization of Cg-Rel, a gene encoding the Crassostrea gigas homolog of Rel/NF-kappaB transcription factors found in insects and mammals [13].

Analytical, diagnostic and therapeutic context of gig

• To gain insight into the evolution of the structure and functions of transforming growth factor (TGF)-beta superfamily members, a cDNA encoding a new member from the bivalve mollusc Crassostrea gigas named mGDF (molluscan growth and differentiation factor) was identified by PCR using degenerate primers [14].
• 1170-1176) from X-ray crystallography on the structure of a closely related enzyme from Desulfovibrio gigas [15].

References