GTPCH, GTP cyclohydrolase, GTP cyclohydrolase I, unpigmented, upi
Gene model reviewed during 5.39
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.48
1.75, 1.7 (northern blot)
None of the polypeptides share 100% sequence identity.
308, 274 (aa); 40, 39 (kD observed); 34, 30 (kD predicted)
Toroid-shaped homodecamer, composed of two pentamers of five dimers.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Pu using the Feature Mapper tool.
The Pu protein is detected in the nurse cell cytoplasm in stage S10B of oogenesis, and has been transferred to granules in the oocyte cytoplasm at stage S14 of oogenesis. The level of Pu protein is high in the unfertilized egg, declines through early embryogenesis, and is not detected after cellularization.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Pu in GBrowse 2
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Recessive alleles are superscripted 'r' and revertants 'rv'.
The expression pattern of Pu protein in wild-type and mutant embryos has been determined.
Pu gene product is required for a vital functions at two distinct stages of embryogenesis and a pigmentation function in the eyes of young adults.
Enzyme assays were used to determine if Aph and sepiapterin were effective inhibitors of Pu gene product.
Germline clone analysis demonstrates that a product of the Pu locus is required during embryogenesis. The germline function of Pu is autonomous. Embryos derived from homozygous null clones can be rescued by a wild type paternal gene product.
A mutant of Pu has been shown to influence the level of in vivo detectable 5,6,7,8-tetrahydroperin and 5,6,7,8-tetrahydrobioperin.
A morphological analysis of Pu has been performed to define the early functions of the Pu locus. Pu has a late embryonic phenotype: loss of Pu function and an early embryonic phenotype: maternal and zygotic components and a segmentation pattern defect.
Mutations at this locus comprise a complex of viable and lethal, recessive and dominant, complementing and noncomplementing alleles with different stage and tissue specific defects. A complementation map has been constructed, but recombinational fine structure has not been determined.
The structural gene for guanosine triphosphate 7,8-8,9-dehydrolase = GTP cyclohydrolase (GTP CH) which catalyzes the first step in pteridine biosynthesis, the conversion of GTP to dihydroneopterin with the release of formic acid; GTP CH activity proportional to the number of Pu+ alleles. Purification and characterization by Weisberg and O'Donnell (1986); the active complex has an apparent molecular mass of 575,000 daltons comprised of 39,000-dalton subunits. Developmentally regulated with a short-lived activity peak at or shortly before eclosion; 80-90% of activity found in the head; activity not detectable in embryos. Dominant alleles are embryonic lethal as homozygotes and in heterozygotes produce dilute purple eye color; Appear to be antimorphic in that GTP CH activity in heterozygotes reduced to less than the 50% normal levels observed in deficiency heterozygotes, at least in adult tissues and is but 80% normal in genotypes that carry, in addition to the mutant allele, two doses of Pu+. Most are associated with a chromosome rearrangement with one breakpoint in 57 and the other in or near centric heterochromatin. A few recessive alleles are viable and fertile and exhibit reduced GTP CH activity in the head but normal or near-normal levels in prepupae and adult body; however, the majority are embryonic lethals and have reduced activity in prepupae, adult body and head when heterozygous with viable alleles; rare lethal alleles are defective in neither eye-pigment production nor in postembryonic enzyme activity. Viable alleles complement lethal alleles for viability, at least partially; in combination with each other and with lethal alleles they display a wide range of eye pigmentation; some pairs of lethal alleles complement fully or partially for both viability and eye color; prepupal enzyme levels are variably reduced in these combinations in ways that are uncorrelated with survival; heteroallelic survivors are fertile; heteroallelic survival markedly reduced or absent when reared at 16oC. Homozygous deficiencies Df(2R)F36 die as fully formed larvae, but prior to hatching; mouth parts and setae completely unpigmented; setae and sensory structures poorly differentiated; cuticle thin and fragile; head involution and differentiation frequently incomplete, beginning at the time of germ-band shortening. Class II mutants display variably similar phenotypes as do class III alleles, but to a less severe extent. 50% of class V mutants die before blastoderm, the remaining 50% dying during late embryogenesis, but with fully pigmented mouth parts and setae and with normal head development; fusions and deletions of abdominal denticle belts, or the normal number of belts, but all of identically abnormal structure, retaining only the two posterior setal rows; preblastoderm nuclear divisions asynchronous, abnormally distributed in embryos, and nuclei misshapen (Reynolds and O'Donnell, 1987). Embryos homozygous for class IV alleles resemble class V mutants, but with additional features characteristic of class II embryos, including unpigmented setae and mouth parts. In crosses of class V bearing genotypes to Df(2R)F36/+, the Df(2R)F36/Pu embryos resemble class V embryos when the deficiency is maternally inherited and deficiency homozygotes when the Pu allele is maternally inherited.