ma-l, bronzy, bz
Please see the JBrowse view of Dmel\mal for information on other features
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.50
Gene model reviewed during 5.55
737 (aa)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\mal using the Feature Mapper tool.
Comment: maternally deposited
GBrowse - Visual display of RNA-Seq signals
View Dmel\mal in GBrowse 21-64
1-64.6
1-64.8
1-64.9 +/- 0.2
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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.
Source for identity of: mal CG1692
The alleles of mal have been mapped both by complementation for eye color and by recombination. Five complementation units have been defined (Chovnick, Finnerty, Schalet and Duck, 1969) and malC2 said to define a sixth (Bentley and Williamson, 1982). There is but a single lethal complementation group in heteroallelic combinations raised on purine-enriched medium. Recombinational mapping utilized purine sensitivity to select for mal+ recombinants (Finnerty, Duck and Chovnick, 1970). Maps co-linear.
Lesions in mal affect eye pigmentation to a small extent only.
Mutations at mal are fully viable, have a maternal effect phenotype and exhibit a brownish eye colour. Larval Malpighian tubules can be short, bloated and irregularly formed.
Aldehyde oxidase deficient mutants of mal have appreciable levels of aldehyde oxidase cross-reacting material in both larval haemolymph and adult extracts.
Rocket immunoelectrophoresis was used to estimate xanthine dehydrogenase cross-reacting material (XDH-CRM). Results show high levels of XDH-CRM in mutant mal flies, this suggests that the primary effects of the mutant gene is on the function of XDH protein rather than its accumulation.
Mutations of mal exhibit the same levels of sulfite oxidase activity as wild-type flies. Xanthine dehydrogenase and aldehyde oxidase cannot be detected, but there are wild-type levels of alcohol dehydrogenase.
Brownish eye color resulting from reduction in the red (drosopterin) pigments. Larval Malpighian tubes short, bloated, irregularly formed and contain yellow to orange pteridine globules (Schwinck, 1960). mal is nonautonomous for eye color in mosaics with wild-type tissue (Glassman, 1957) and in transplants of mal eyes into wild-type hosts (Ursprung, 1961). Activities of three molybdo-enzymes reduced or absent: aldehyde oxidase = AO (Courtright, 1967), pyridoxal oxidase = PO (Forrest, Hanley and Lagowski, 1961) and xanthine dehydrogenase = XDH (Forrest, Glassman and Mitchell, 1956) (Glassman and Mitchell, 1959). Measurements of cross-reacting material (e.g., Browder, Wilkes and Tucker, 1982; Browder, Tucker and Wilkes, 1982) show 75% and 50% normal levels of AO CRM in larval hemolymph and adult extracts respectively and 105% normal level of XDH CRM (see also Warner, Watts and Finnerty, 1980). Activity of a fourth molybdo-enzyme, sulfite oxidase, is unaffected by mal (Bogart and Bernini, 1981). Furthermore, unlike mutants in genes thought to be involved with the function of molybdenum cofactor, e.g. cin and lxd, the effects of mal not alleviated by administration of molybdenum; XDH cross reacting material (CRM) isolated from mal flies contains molybdenum (Andres, 1976); mal flies contain high levels of molybdenum cofactor by Neurospora nitrate reductase activation assay (Warner and Finnerty, 1981). Accumulation of enzyme substrates (Forrest, Glassman and Mitchell, 1956; Glassman and Mitchell, 1959; Glassman and McLean, 1962) may account for the reported increase in uricase activity (Friedman, 1970). The absence of XDH activity renders mal flies sensitive to exogenously supplied purine (Glassman, 1965), which has been used in selective schemes (Finnerty, Duck and Chovnick, 1970); the cell autonomy of mal with respect to AO activity provides the basis of a staining procedure for differentiating mal from mal+ tissue in mosaics (Janning, 1972). mal offspring of mal+ mothers appear normal in both eye color and Malpighian-tube morphology (Glassman and Mitchell, 1959; Schwinck, 1960); mal+ activity observed in germ line as AO activity (Marsh and Wieschaus, 1977) and maternally inherited XDH activity in mal offspring detectable until second day of pupal stage (Browder and Williamson, 1976). Maternal effect suppressed if offspring are also homozygous for lxd (Courtright, 1975). Interallelic complementation in females of constitution mal1/malF1; eye color and Malpighian-tube morphology appear normal, but XDH activity about 10% normal (Glassman and Mitchell, 1959; Schwinck, 1960); complementation not seen in flies raised at 29oC and reduced in flies that are also homozygous for lxd (Courtright, 1975); physical properties of XDH and AO altered in different heteroallelic combinations (Finnerty, McCarron and Johnson, 1979; Finnerty and Johnson, 1979). mal1, malF1, and malF3 complement for eye color in all pairwise combinations; however, malF1 malF3/mal1 is mutant. mal and ry extracts complement to produce XDH activity (Glassman, 1962); they do not complement intercellularly in vivo, however, since reciprocal eye-disk or Malpighian-tube transplants reported to behave autonomously with respect to drosopterin formation (Schwinck, 1960; Schwinck, 1963).
