Transport defects as the physiological basis for eye color mutants of Drosophila melanogaster

Sullivan, David T.; Sullivan, Marie C.

doi:10.1007/bf00484918

Cited by 132 publications

(94 citation statements)

References 13 publications

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“…The predicted protein encoded by these transcripts showed striking similarity to that encoded by the Drosophila white and scalier genes and to members of a family of active transport proteins. This finding was in accordance with the expected functions of brown, white, and scarlet in transport of pigment precursors (Sullivan and Sullivan 1975) and their hypothesized protein-protein interactions (Farmer and Fairbanks 1986). A genomic clone (designated 1111 in Dreesen et al 1988) derived from a cosmid library made from DNA of the wild-type Sevelen strain was used for further studies.…”

Section: The Functional Brown Gene Lies Within An 84-kb Genomic Segmentsupporting

confidence: 89%

A pairing-sensitive element that mediates trans-inactivation is associated with the Drosophila brown gene.

Dreesen¹,

Henikoff²,

Loughney³

1991

Genes Dev.

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Position-effect variegation in Drosophila is the mosaic expression of a gene juxtaposed to heterochromatin by chromosome rearrangement. The brown (bw +) gene is unusual in that variegating mutations are dominant, causing "trans-inactivation" of the homologous allele. We show that copies of bw + transposed to ectopic sites are not trans-inactivated by rearrangements affecting the endogenous gene. However, when position-effect variegation is induced on an ectopic copy by chromosome rearrangement, the allele on its paired homolog is trans-inactivated, whereas other copies of bw + are not. This confirms that trans-inactivation is "chromosome local" and maps the responsive element to the immediate vicinity of brown. Subsequent P-transposase-induced deletions within the ectopic copy in cis to the rearrangement breakpoint caused partial suppression of trans-inactivation. Surprisingly, the amount of suppression was correlated with deletion size, with some degree of trans-inactivation persisting even when the P[bw +] transposon was completely excised. The chromosome-local nature of the phenomenon and its extreme sensitivity to small disruptions of somatic pairing leads to a model in which a regulator of the brown gene is inactivated by direct contact with heterochromatic proteins.[Key Words: Position-effect variegation; Drosophila; somatic pairing; in vivo deletion mappingl Received November 21, 1990; accepted December 18, 1990.A common class of mutations induced by ionizing radiation in Drosophila are the variegating position effects. These are generally caused by chromosomal rearrangements placing euchromatic genes in the vicinity of heterochromatin, the compacted regions of chromosomes that remain condensed during most of the cell cycle (for review, see Spofford 1976; Henikoff 1990). The variegated phenotype is caused by reduction in gene expression in some cells but not in others, evidently as a result of transcriptional inactivation (Henikoff 1981;Rushlow et al. 1984;Henikoff and Dreesen 1989). Consistent with this interpretation, position-effect variegation of nearly all genes is recessive, implying that inactivation of one copy of a gene in cis has no effect on the copy in trans. However, variegated position effects on a few genes, including the brown (bw +) gene, are dominant (Muller 1932;Slatis 1955;Stem and Kodani 1955;Henikoff 1979;O'Donnell et al. 1989).Recently, we showed that dominant position-effect variegation of brown involves a sharp reduction in mRNA accumulation from both copies of the gene, the copy in cis to the rearrangement breakpoint (cis-inactivation) and the copy in trans (trans-inactivation). We proposed a somatic pairing model in which the brown gene region, inactivated by virtue of its juxtaposition to heterochromatin, could transmit the inactivated state to the copy of brown in trans. Evidence for this model was the sensitivity of trans-inactivation to chromosome configurations that are expected to disrupt somatic pairing in the vicinity of the brown gene.The somatic pairing model makes sev...

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Section: The Functional Brown Gene Lies Within An 84-kb Genomic Segmentsupporting

confidence: 89%

A pairing-sensitive element that mediates trans-inactivation is associated with the Drosophila brown gene.

Dreesen¹,

Henikoff²,

Loughney³

1991

Genes Dev.

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“…In Drosophila, W is essential to both pigment pathways (Sullivan and Sullivan 1975;Sullivan et al 1979;Summers et al 1982), so it was not surprising to see that all individuals injected with Tcw dsRNA as larvae lacked eye pigmentation as pupae and adults ( Figure 2B). Moreover, our results for Tcst were also similar to that previously reported (Broehan et al 2013).…”

Section: Rna Interferencementioning

confidence: 99%

“…The transport protein, White (W), works with its paralog, Scarlet (St), to import precursors of ommochrome pigments (Sullivan and Sullivan 1975;Tearle et al 1989). Because these pigments provide brown coloration in Drosophila, failure of St function results in bright red eyes.…”

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confidence: 99%

The ABCs of Eye Color inTribolium castaneum: Orthologs of theDrosophila white,scarlet, andbrownGenes

et al. 2015

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In Drosophila melanogaster, each of the three paralogous ABC transporters, White, Scarlet and Brown, is required for normal pigmentation of the compound eye. We have cloned the three orthologous genes from the beetle Tribolium castaneum. Conceptual translations of Tribolium white (Tcw), scarlet (Tcst), and brown (Tcbw) are 51, 48, and 32% identical to their respective Drosophila counterparts. We have identified loss-of-eye-pigment strains that bear mutations in Tcw and Tcst: the Tcw gene in the ivory (i) strain carries a single-base transversion, which leads to an E / D amino-acid substitution in the highly conserved Walker B motif, while the Tcst gene in the pearl (p) strain has a deletion resulting in incorporation of a premature stop codon. In light of these findings, the mutant strains i and p are herein renamed white ivory (w i ) and scarlet pearl (st p ), respectively. In addition, RNA inhibition of Tcw and Tcst recapitulates the mutant phenotypes, confirming the roles of these genes in normal eye pigmentation, while RNA interference of Tcbw provides further evidence that it has no role in eye pigmentation in Tribolium. We also consider the evolutionary implications of our findings.

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“…Serotonin synthesis begins with hydroxylation of tryptophan, which is also the initial substrate for production of brown pigment xanthommatin, a process requiring White (Sullivan and Sullivan 1975). Serotonin content is greatly reduced in the mutant strain w1118 (Borycz et al 2008;Sitaraman et al 2008).…”

Section: Knockdown Of W In Subsets Of Serotonin Neurons Was Sufficienmentioning

confidence: 99%

“…The White protein is involved in the uptake of precursors into granules for the synthesis of pteridine (red) and ommochrome (brown) pigments (O'Hare et al 1984;Dreesen et al 1988;Tearle et al 1989). In the Malpighian tubule, the w + transport system is associated with the accumulation of intracellular 3-hydroxykynurenine and cyclic guanosine monophosphate (cGMP) in the granules/vesicles (Sullivan and Sullivan 1975;Evans et al 2008). The w + transport system also transports the pigment precursors, guanine and tryptophan, crossing cytoplasmic membranes to contribute to pigment synthesis (Green 1949;Sullivan et al 1979;Sullivan et al 1980;Ferré et al 1986).…”

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confidence: 99%

Timing of Locomotor Recovery from Anoxia Modulated by the white Gene in Drosophila

Xiao

Robertson

2016

Genetics

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Locomotor recovery from anoxia follows the restoration of disordered ion distributions and neuronal excitability. The time taken for locomotor recovery after 30 sec anoxia (around 10 min) is longer than the time for the propagation of action potentials to be restored (,1 min) in Drosophila wild type. We report here that the white (w) gene modulates the timing of locomotor recovery. Wildtype flies displayed fast and consistent recovery of locomotion from anoxia, whereas mutants of w showed significantly delayed and more variable recovery. Genetic analysis including serial backcrossing revealed a strong association between the w locus and the timing of locomotor recovery, and haplo-insufficient function of w + in promoting fast recovery. The locomotor recovery phenotype was independent of classic eye pigmentation, although both are associated with the w gene. Introducing up to four copies of mini-white (mw + ) into w1118 was insufficient to promote fast and consistent locomotor recovery. However, flies carrying w + duplicated to the Y chromosome showed wild-type-like fast locomotor recovery. Furthermore, Knockdown of w by RNA interference (RNAi) in neurons but not glia delayed locomotor recovery, and specifically, knockdown of w in subsets of serotonin neurons was sufficient to delay the locomotor recovery. These data reveal an additional role for w in modulating the timing of locomotor recovery from anoxia.

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Transport defects as the physiological basis for eye color mutants of Drosophila melanogaster

Cited by 132 publications

References 13 publications

A pairing-sensitive element that mediates trans-inactivation is associated with the Drosophila brown gene.

A pairing-sensitive element that mediates trans-inactivation is associated with the Drosophila brown gene.

The ABCs of Eye Color inTribolium castaneum: Orthologs of theDrosophila white,scarlet, andbrownGenes

Timing of Locomotor Recovery from Anoxia Modulated by the white Gene in Drosophila

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