DNA-protein interactions: genome-wide binding profile assayed for gt protein in 2-3 hr embryos; see BDTNP1_TFBS_gt collection report.

S2 cells treated with dsRNA generated against this gene show reduced phagocytosis of Candida albicans compared to untreated cells.

Mutations in gt cause defects in the labial segment (the most posterior cephalic segment), and in the labral segment (the most anterior cephalic segment, adjacent to the unsegmented anterior tip).

Mutant embryos lack the corpus cardiacum.

In a sample of 79 genes with multiple introns, 33 showed significant heterogeneity in G+C content among introns of the same gene and significant positive correspondence between the intron and the third codon position G+C content within genes. These results are consistent with selection adding against preferred codons at the start of genes.

The gt transcriptional repressor defines the anterior border of stripe 2 of eve. A single gt binding site maps 50bp from the nearest activator site in the eve stripe 2 enhancer.

Gene product is known to regulate Kr CD (cis acting control element) expression.

Substitution of 5 amino acids in the vertebrate VBP bZIP factor that differ between the Drosophila gt bZIP factor and vertebrate PAR bZIP factors indicates that the fork region, which bridges the basic and leucine zipper domains, contributes to half-site specificity.

The abdominal cad domain is required to activate the gap genes kni and gt.

gt is responsible for the posterior boundary of h stripe 5.

E(z) is required to maintain the expression domain of kni and gt initiated by the maternal hb gradient.

Muscle phenotype of mutants studied using polarised light microscopy and antibody staining to detect Mhc-lacZ reporter gene expression in muscles.

Expression of prd depends on activation by gap gene hb, Kr, kni and gt products. Primary pair rule gene products act primarily in subsequent modulation rather than activation of prd stripes. Factors activating prd expression in the pair rule mode interact with those activating it along the dorso-ventral axis.

The role of gt in the regulation of run mRNA expression in the early embryo has been investigated.

Examination of conserved tracts in the D.virilis and D.melanogaster h gene promoters identified potential ftz-f1, Kr and gt binding sites. Kr and gt products establish the anterior and posterior borders of h stripe 5, respectively, through spatial repression.

gt has been cloned and characterised. Its interactions with Kr and kni have been studied.

The gene products of bcd, hb, Kr and gt all bind within the 480bp region that is necessary and sufficient for the expression of eve stripe 2. gt is involved in refining the anterior border of the stripe.

Anterior gt expression is bcd-dependent and not repressed by maternal hb. Posterior expression is independent of bcd and repressed by hb. These results strongly suggest that anterior and posterior domains of gt expression are controlled by two separate regulatory elements that act independently and respond to different regulatory proteins. gt has a strong negative effect on kni expression.

Regulatory interactions of gap genes modulate gt expression but are not required for its initiation in the embryo.

It has been shown that Kr and gt are expressed in complementary, non-overlapping sets of cells in the early embryo. Interactions between the two genes have been studied.

Mutations in zygotic cardinal gene gt interact with RpII140^wimp.

gt protein directly regulates the expression of eve stripe 2 expression by DNA binding to the stripe 2 promoter element.

Zygotically active locus involved in the terminal developmental program in the embryo.

gt mutants exhibit deletions of the head and abdomen.

The gt transcription unit has been identified: the temporal and spatial pattern of expression investigated. Mutants in Kr, kni and hb affect the posterior gt expression domain but mutants in eve do not affect gt expression.

Mutant embryos exhibit normal Dfd expression.

Germ line clonal analysis indicates that gt has no maternal effect.

gt mutants display defects in head and in the fifth through seventh abdominal segment.

Used by Bridges (1935) in the construction of salivary chromosome maps. Preliminary evidence of interallelic complementation with respect to phenotype and viability presented by Duttagupta, Das and Dutta (1984).

Larval development 4 days longer than normal resulting in giant larvae, pupae, and imagos. Adult weight 1.7 times normal; increased size caused by increase in cell size and not cell number (Simpson and Morata, 1980). Pupariation delayed owing to delayed increase in ecdysteroid titers; level reached at pupariation lower than normal; pupal interval of normal length (Schwartz, Imberski and Kelly, 1984). Not all genetically giant flies show the giant character, the rest have normal size; distribution sharply bimodal. Percentage giant greatest in well-fed cultures, also raised by modifying action of bb¹¹. Penetrance of viable alleles enhanced in heterozygotes with lethal alleles and deficiencies; viability decreased (Kaufman, 1972). Abnormalities in DNA metabolism found in homo- or heteroallelic third instar gt females (Narachi and Boyd, 1985). Salivary gland chromosomes of double thickness in some cells (Bridges, 1935). Feulgen staining shows extra round of DNA synthesis; polytene chromosome can be analyzed in gt/Df larvae (Kaufman, 1972). Embryos carrying lethal giant mutations have defects in the anterior and the posterior domains (Petschek, Perrimon and Mahowald, 1987; Mohler, Eldon and Pirrotta, 1989). Posterior compartment of the labial segment deleted from blastoderm; cell death at germ-band elongation deletes anterior compartments of abdominal segments 5-7. Posterior-compartment structures of A5-7 in the peripheral nervous system fuse in mature embryos (Petschek and Mahowald, 1980). Hemizygotes for lethal alleles, gt^13z and gt^X11, fail to hatch (Kaufman, 1973); denticle belts of the fifth through the seventh abdominal segments partially or completely absent; internally corresponding neuromeres absent; eight abdominal neuromeres disconnected from remainder. Head does not complete involution, shows characteristic 'buttonhead' phenotype with ventral skeleton extruded from the anterior end of the larva (Mohler, Eldon and Pirrotta, 1989), pharynx and pharyngeal chitinized sclerites shorter and brain lobes somewhat smaller than normal; extensive cell death in epidermal and neural components of embryo (Honisch and Campos-Ortega, 1982). Effect cell autonomous in mosaic embryos. (Gergen and Wieschaus, 1986). Germline clones viable (Garcia-Bellido and Robbins, 1983). gt stocks (homo- or heteroallelic) show an increase in the frequency of spontaneous mutations, including deletions of y and w loci (Green, 1982); these stocks also synthesize DNA of a reduced molecular weight and show many single-strand and double-strand breaks, suggesting abnormalities in DNA metabolism (Narachi and Boyd, 1985).