The Location of a New Second Chromosome Eye Colour Gene in Drosophila Melanogaster

Waaler, Georg H. M.

doi:10.1111/j.1601-5223.1921.tb02636.x

Cited by 5 publications

(3 citation statements)

References 1 publication

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“…The bw gene is a classic gene first described in 1921 by Waaler, 27 which causes the eyes to be brown rather than red and encodes an 5). For example, Drosophila pseudoobscura has three of the extended amino acids found in w 1118 ; iso-2; iso-3 and Drosophila mojavenais has four of them.…”

Section: Resultsmentioning

confidence: 99%

A program for annotating and predicting the effects of single nucleotide polymorphisms, SnpEff

Cingolani

Platts

Wang

et al. 2012

Fly

9,370

7,617

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We describe a new computer program, SnpEff, for rapidly categorizing the effects of variants in genome sequences. Once a genome is sequenced, SnpEff annotates variants based on their genomic locations and predicts coding effects. Annotated genomic locations include intronic, untranslated region, upstream, downstream, splice site, or intergenic regions. Coding effects such as synonymous or non-synonymous amino acid replacement, start codon gains or losses, stop codon gains or losses, or frame shifts can be predicted. Here the use of SnpEff is illustrated by annotating ~356,660 candidate SNPs in ~117 Mb unique sequences, representing a substitution rate of ~1/305 nucleotides, between the Drosophila melanogaster w(1118); iso-2; iso-3 strain and the reference y(1); cn(1) bw(1) sp(1) strain. We show that ~15,842 SNPs are synonymous and ~4,467 SNPs are non-synonymous (N/S ~0.28). The remaining SNPs are in other categories, such as stop codon gains (38 SNPs), stop codon losses (8 SNPs), and start codon gains (297 SNPs) in the 5'UTR. We found, as expected, that the SNP frequency is proportional to the recombination frequency (i.e., highest in the middle of chromosome arms). We also found that start-gain or stop-lost SNPs in Drosophila melanogaster often result in additions of N-terminal or C-terminal amino acids that are conserved in other Drosophila species. It appears that the 5' and 3' UTRs are reservoirs for genetic variations that changes the termini of proteins during evolution of the Drosophila genus. As genome sequencing is becoming inexpensive and routine, SnpEff enables rapid analyses of whole-genome sequencing data to be performed by an individual laboratory.

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Section: Resultsmentioning

confidence: 99%

A program for annotating and predicting the effects of single nucleotide polymorphisms, SnpEff

Cingolani

Platts

Wang

et al. 2012

Fly

9,370

7,617

View full text Add to dashboard Cite

show abstract

“…Flies carrying cinnabar, brown (cn, bw) double mutations in a w + background were generated. These flies (w + ; cn,bw) were white-eyed ( Figure 3A) due to complete blockage of both pteridine and ommochrome pigment pathways (WAALER 1921;WARD 1923;NOLTE 1954;GHOSH and FORREST 1967;DREESEN et al 1988). There was no difference of TR between w + ; cn,bw flies (median 579.0 s, IQR 467.8 -674.8 s, n = 16) and CS (median 494.0 s, IQR 455.0 -555.5 s, n = 16) ( Figure 3B).…”

Section: Independent Phenotypes Between Locomotor Recovery From Anoximentioning

confidence: 99%

Timing of locomotor recovery modulated by thewhitegene inDrosophila

Xiao

Robertson

2015

Preprint

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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 s anoxia (around 10 min) is longer than the time for the propagation of action potentials to be restored (less than 1 min) in Drosophila wild-type. We report here that the white (w) gene modulates the timing of locomotor recovery. Wild-type flies displayed fast and consistent recovery of locomotion from anoxia, whereas mutants of w showed significantly delayed 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 locomotor 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 Y chromosome showed wild-type-like fast locomotor recovery. Furthermore, RNAi knockdown of w in neurons but not glia delayed locomotor recovery, and specifically, knockdown of w in putative 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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“…Flies carrying cinnabar, brown (cn, bw) double mutations in a w + background were generated. These flies (w + ; cn,bw) were white-eyed ( Figure 3A) due to complete blockage of both pteridine and ommochrome pigment pathways (Waaler 1921;Ward 1923;Nolte 1954;Ghosh and Forrest 1967;Dreesen et al 1988). There was no difference of TR between w + ; cn,bw flies (median 579.0 sec, IQR 467.8-674.8 sec, n = 16) and CS (median 494.0 sec, IQR 455.0-555.5 sec, n = 16) ( Figure 3B).…”

Section: Mutants Of W Showed Delayed Locomotor Recovery From Anoxiamentioning

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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The Location of a New Second Chromosome Eye Colour Gene in Drosophila Melanogaster

Cited by 5 publications

References 1 publication

A program for annotating and predicting the effects of single nucleotide polymorphisms, SnpEff

A program for annotating and predicting the effects of single nucleotide polymorphisms, SnpEff

Timing of locomotor recovery modulated by thewhitegene inDrosophila

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

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