Application of a time-delay neural network to promoter annotation in the Drosophila melanogaster genome

Reese, Martin G.

doi:10.1016/s0097-8485(01)00099-7

Cited by 798 publications

(620 citation statements)

References 18 publications

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“…Putative promoters were identified using the Neural Network Promoter Prediction Program (Reese 2001; http://www.fruitfly.org/seq_tools/promoter.html) with a cutoff score of 0.70.…”

Section: Rna Isolation and Complementary Dna Synthesismentioning

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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“…Putative promoters were identified using the Neural Network Promoter Prediction Program (Reese 2001; http://www.fruitfly.org/seq_tools/promoter.html) with a cutoff score of 0.70.…”

Section: Rna Isolation and Complementary Dna Synthesismentioning

confidence: 99%

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

et al. 2015

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“…The variation was not reported in the NCBI dbSNP, and parental DNA was not available for screening. The promoter region of PRKD1 was analysed using two software programs (BDGP Neural Network promoter prediction software, http://www.fruitfly.org/seq_tools/ promoter.html 27 and Promo 3.0, http://alggen.lsi.upc.es/cgi-bin/ promo_v3/promo/promoinit.cgi?dirDB=TF_8.3 ). 28 There were no differences between the predictions from the wild-type sequence and Figure 1 14q12 microdeletions excluding coding region of FOXG1.…”

Section: Chromosomal Microarray Analysismentioning

confidence: 99%

14q12 microdeletions excluding FOXG1 give rise to a congenital variant Rett syndrome-like phenotype

Ellaway

Bettella

et al. 2012

Eur J Hum Genet

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Rett syndrome is a clinically defined neurodevelopmental disorder almost exclusively affecting females. Usually sporadic, Rett syndrome is caused by mutations in the X-linked MECP2 gene in B90-95% of classic cases and 40-60% of individuals with atypical Rett syndrome. Mutations in the CDKL5 gene have been associated with the early-onset seizure variant of Rett syndrome and mutations in FOXG1 have been associated with the congenital Rett syndrome variant. We report the clinical features and array CGH findings of three atypical Rett syndrome patients who had severe intellectual impairment, early-onset developmental delay, postnatal microcephaly and hypotonia. In addition, the females had a seizure disorder, agenesis of the corpus callosum and subtle dysmorphism. All three were found to have an interstitial deletion of 14q12. The deleted region in common included the PRKD1 gene but not the FOXG1 gene. Gene expression analysis suggested a decrease in FOXG1 levels in two of the patients. Screening of 32 atypical Rett syndrome patients did not identify any pathogenic mutations in the PRKD1 gene, although a previously reported frameshift mutation affecting FOXG1 (c.256dupC, p.Gln86ProfsX35) was identified in a patient with the congenital Rett syndrome variant. There is phenotypic overlap between congenital Rett syndrome variants with FOXG1 mutations and the clinical presentation of our three patients with this 14q12 microdeletion, not encompassing the FOXG1 gene. We propose that the primary defect in these patients is misregulation of the FOXG1 gene rather than a primary abnormality of PRKD1.

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“…Mutations affecting DGAD2 expression in the cuticle but not the nervous system could be a possible explanation for the difference in the visual phenotype between ebony and black. The genomic sequence was analysed for potential transcription start-sites and two with equal likelihood (0.99) were predicted by the program (Reese, 2001). The first site is at À143 bp, and the second at +77 bp from the first putative translation start codon in the cDNA.…”

Section: S R T H R H -P R F T G V E R a D S V T W N P H K 321 Fel Gamentioning

confidence: 99%

The Drosophila black enigma: The molecular and behavioural characterization of the black1 mutant allele

Phillips

Smart

Strauß³

et al. 2005

Gene

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The cuticular melanization phenotype of black flies is rescued by h-alanine, but h-alanine production, by aspartate decarboxylation, was reported to be normal in assays of black mutants, and although black/Dgad2 is expressed in the lamina, the first optic ganglion, no electroretinogram (ERG) or other visual defect has been demonstrated in black flies. The purpose of this study was to investigate the black gene, and protein, in black 1 mutants of Drosophila melanogaster in order to resolve the apparent paradox of the black phenotype. Using black 1 mutant flies we show that (1) aspartate decarboxylase activity is significantly reduced in adults and at puparium formation, consistent with defects in cuticular and non-cuticular processes, (2) that the black 1 mutation is a frameshift, and black 1 flies are nulls for the black/ DGAD2 protein, and (3) that behavioural experiments using Buridan's paradigm, demonstrate that black responds abnormally to visual cues. No ERG, or target recognition defects can be demonstrated suggesting a problem with higher order visual functions in black mutants. D

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Application of a time-delay neural network to promoter annotation in the Drosophila melanogaster genome

Cited by 798 publications

References 18 publications

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

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

14q12 microdeletions excluding FOXG1 give rise to a congenital variant Rett syndrome-like phenotype

The Drosophila black enigma: The molecular and behavioural characterization of the black1 mutant allele

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