Pdxk¹ homozygous third instar larvae exhibit chromosomal aberrations (such as autosomal chromatid deletion, isochromatid deletion and isochromatid deletion at the level of centromere) in neuroblasts when compared to controls.

Mitotic cells from colchicine-treated Pdxk¹ mutant brains display ~6% chromosome aberrations (CABs), compared to ~0,5% in wild type cells. A significantly higher proportion of CABs is seen in Pdxk¹/Df(3L)AC1 mutant cells.

Feeding Pdxk¹ mutant larvae food that has been supplemented with Pyridoxal 5'-phosphate (PLP) in 4% sucrose suppresses the increased frequency of colchicine-induced chromosome aberrations (CABs) seen on standard food to wild type levels. Conversely, supplementing the food solely with 4% sucrose enhances the phenotypes; a 3-fold increase in CAB frequency is seen.

Dissecting the brains of Pdxk¹ mutant third instar larvae and incubating them in medium supplemented with 1% glucose causes a substantial increase in the number of colchicine-induced chromosome aberrations (CABs) compared with controls incubated in saline. An even greater increase in CAB frequency is seen when larval brains are incubated in saline supplemented with 1% fructose. Neither sucrose or fructose increases CAB frequency in wild type flies. The effects of both sugars are completely suppressed when 1 mM Pyridoxal 5'-phosphate (PLP) is added to the medium.

In Pdxk¹ colchicine-treated mutant brains exposed to high glucose concentrations, the frequency of cells with chromosome aberrations (CABs) increases with an increasing intracellular glucose concentration (IGC). Treatments of 1% and 5% glucose result in increased CABS in Pdxk¹ mutants, but no increase in CABS is seen in wild type until treatment with 10% glucose. Pdxk¹ mutant brain cells have significantly higher numbers of CABs than wild type cells with a comparable IGC, with mutant brains showing a higher frequency of metaphases with damaged chromosomes. In brains with high IGC approximately 10% of the metaphases with more than 5 CABs show an extensive chromosome fragmentation. Adding tyrosine to the incubation medium does not increase the frequency of CABs compared to incubation in glucose alone. A reduction in CAB frequency is also seen with α-lipoic acid (ALA), both in the presence or absence of glucose.

The loss of recognisable spindle structures seen in colchicine-treated wild type and Pdxk¹ mutant brains is not seen in Pdxk¹ mutant brains incubated in 1% glucose. Glucose-treated mutant cells contain several anaphases, and these cells display many mitotic spindles with a slightly reduced microtubule density but otherwise normal. The addition of 1mM Pyridoxal 5'-phosphate (PLP) or 1.7 mM tyrosine to the medium partially suppresses this phenotype but no change in suppression is seen with 1.7 mM glycine.

Pdxk¹ mutant larvae exhibit lower dTTP and higher dUTP levels compared with wild type controls. Pyridoxal 5'-phosphate (PLP) level in Pdxk¹ mutants is approximately 50% of that in wild type. However Pdxk¹ mutant larval brains show weak sensitivity to hydroxyurea; a similar frequency of colchicine-induced chromosome aberrations is seen in hydroxyurea treated Pdxk¹ mutants as in wild type and untreated Pdxk¹ mutant controls.

Both untreated and glucose treated Pdxk¹ mutant brains consistently exhibit higher frequencies of Advanced Glycation End products (AGEs) compared to controls. The addition of Pyridoxal 5'-phosphate (PLP) suppresses this effect. Addition of α-lipoic acid (ALA) also partially reduces the frequency of AGE positive cells.

The hemolymph of Pdxk¹ mutant larvae contains nearly twice as much glucose as that of wild type larvae.

Mitotic cells from colchicine-treated Pdxk¹/Pdxk² mutant brains display ~6% chromosome aberrations (CABs), compared to ~0.5% in wild type cells.

Pdxk¹ has nuclear chromosome | third instar larval stage phenotype, suppressible | partially by Hsap\PDXK^{A234G.Tub.Tag:HA}

Pdxk¹ has larval neuroblast | third instar larval stage phenotype, suppressible by Hsap\PDXK^Tub.Tag:HA

Pdxk¹ has nuclear chromosome | third instar larval stage phenotype, suppressible | partially by Hsap\PDXK^{V128I.Tub.Tag:HA}

Pdxk¹ has nuclear chromosome | third instar larval stage phenotype, suppressible | partially by Hsap\PDXK^{H246Q.Tub.Tag:HA}

Pdxk¹ has nuclear chromosome | third instar larval stage phenotype, suppressible | partially by Hsap\PDXK^{D87H.Tub.Tag:HA}

Pdxk¹ has larval neuroblast | third instar larval stage phenotype, suppressible | partially by Hsap\PDXK^{A234G.Tub.Tag:HA}

Pdxk¹ has larval neuroblast | third instar larval stage phenotype, suppressible | partially by Hsap\PDXK^{D87H.Tub.Tag:HA}

Pdxk¹ has larval neuroblast | third instar larval stage phenotype, suppressible | partially by Hsap\PDXK^{V128I.Tub.Tag:HA}

Pdxk¹ has larval neuroblast | third instar larval stage phenotype, suppressible | partially by Hsap\PDXK^{H246Q.Tub.Tag:HA}

Pdxk¹ has nuclear chromosome | third instar larval stage phenotype, suppressible by Hsap\PDXK^Tub.Tag:HA