Psychiatry related information on Tpi

• A missense mutant TIM, TIM-SL, exhibits greater sensitivity to light in both TIM protein disappearance and locomotor activity phase shifting assays [1].

High impact information on Tpi

• Consistent with the fact that light normally suppresses TIM, cryb is an apparent null mutation in a gene encoding Drosophila's version of the blue light receptor cryptochrome [2].
• Analysis of dose response of TIM disappearance in a variety of mutant genotypes suggests cell-autonomous light responses that are largely independent of the canonical visual transduction pathway [1].
• In Tpi-deficient flies and humans, a decrease in ATP levels did not appear to cause the observed phenotypes because ATP levels remained normal [3].
• Instead, we favor the hypothesis that mutations in Tpi lead to an accumulation of methylglyoxal and the consequent enhanced production of advanced glycation end products, which are ultimately responsible for the death and dysfunction of Tpi-deficient neurons [3].
• DNA sequence variation in a 1.1-kb region including the coding portion of the Tpi locus was examined in 25 homozygous third-chromosome lines of Drosophila melanogaster, nine lines of Drosophila simulans, and one line of Drosophila yakuba [4].

Biological context of Tpi

• There is a single copy of the Tpi sequence in the genome of Drosophila, as judged by Southern blots and in situ hybridization to salivary gland chromosomes [5].
• Comparison of C. tarsalis Tpi to that of Drosophila melanogaster revealed that although the two genes had little similarity in the intron and 5' flanking sequences, they were highly similar (73% identity) in their coding sequence [6].
• Biochemical studies demonstrate that mutation of this glycolytic enzyme gene does not result in a bioenergetic deficit, suggesting an alternate cause of enzymopathy associated with TPI impairment [7].
• This is probably caused by impaired nuclear accumulation of TIM(BLIND) protein, which we observed in brain pacemaker neurons and photoreceptor cells of the compound eye. tim(blind) encodes two closely spaced amino acid changes compared to the wild-type TIM protein; one of them is within a putative nuclear export signal of TIM [8].
• We have isolated a missense mutation in the Drosophila sugarkill (sgk) gene that causes phenotypes analogous to symptoms of triosephosphate isomerase (TPI) deficiency, a human familial disease, characterized by anaerobic metabolic dysfunction resulting from pathological missense mutations affecting the encoded TPI protein [7].

Anatomical context of Tpi

• Northern blot analysis of RNA prepared from different developmental stages revealed that Tpi mRNA is present in substantial amounts in oocytes, declines in abundance in early embryos, and begins to increase during mid-embryogenesis [5].
• The per(L) mutation delayed nuclear accumulation in vivo and in our cultured cell system, but without affecting rates of PER/TIM assembly or dissociation [9].

Associations of Tpi with chemical compounds

• Genetic and cytogenetic studies of four glycolytic enzymes in Drosophila melanogaster: aldolase, triosephosphate isomerase, 3-phosphoglycerate kinase, and phosphoglucomutase [10].

Other interactions of Tpi

• The HKA test, which tests imbalance between the intra and interspecific nucleotide variation, showed that the intraspecific nucleotide variation in the Pgi region was much lower than the interspecific variation, while intraspecific variation in the Tpi region was only slightly lower than interspecific variation [11].

Analytical, diagnostic and therapeutic context of Tpi

• In the present study the structure of TIM protein expressed by D. virilis was determined by isolation and sequence analysis of genomic DNA (gDNA) corresponding to the D. virilis tim locus (v tim ) [12].
• Anti-C. tarsalis TPI antibodies cross-reacted with TPIs from other organisms but bands on western blots were most intense with proteins from closely related Dipterans [6].
• Using a degenerate primer corresponding to the amino-terminal sequence of the protein in a polymerase chain reaction (PCR), a cDNA corresponding to the TPI gene (Tpi) was isolated and sequenced [6].

References