<HashMap><database>ENA</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR281/058/SRR28157258/SRR28157258_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR281/059/SRR28157259/SRR28157259_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR281/060/SRR28157260/SRR28157260_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR281/060/SRR28157260/SRR28157260_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR281/059/SRR28157259/SRR28157259_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR281/058/SRR28157258/SRR28157258_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR281/061/SRR28157261/SRR28157261_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR281/061/SRR28157261/SRR28157261_1.fastq.gz</Fastqsanger.gz></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Genomics</omics_type><center_name>University of Missouri</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA1081931</full_dataset_link><long_description>The cell-cell adhesion molecule Fasciclin II (Fas2) has long been studied for its evolutionarily-conserved role in axon guidance. It is also expressed in the follicular epithelium, where together with a similar protein, Neuroglian (Nrg), it helps to drive the reintegration of cells born out of the tissue plane. Remarkably, one Fas2 protein null allele, Fas2G0336, demonstrates a mild reintegration phenotype, whereas work with the classic null allele Fas2EB112 showed more severe epithelial disorganization. These observations raise the question of which allele (if either) causes a bona fide loss of Fas2 protein function. The problem is not only relevant to reintegration but fundamentally important to understanding what this protein does and how it works: Fas2EB112 has been used in at least 37 research articles, and Fas2G0336 in at least three. An obvious solution is that one of the two chromosomes carries a modifier that either suppresses (Fas2G0336) or enhances (Fas2EB112) phenotypic severity. We find not only the latter to be the case, but identify the enhancing mutation as Nrg14, also a classic null allele.</long_description><repository>ENA</repository><description_synonyms>CT12301, flies, Antemortem Diagnoses, Fas 2, Antemortem Diagnosis, anon-EST:Liang-1.60, True, l(1)G0336, Fasii, FasII, CG3665, FAS2, Diagnosis, l(1)G0293, Examination and Diagnoses, Diagnoses, DmelCG3665, Allelomorphs., lsd1, Postmortem, Examinations and Diagnoses, fas II, EG:EG0007.3, FascII, fas2, Fas II, Antemortem, Postmortem Diagnosis, Flies, Diagnoses and Examination, NFB1, Postmortem Diagnoses, True Flies, l(1)G0032, mAb 1D4, MUB3_15, True Fly, Fly, MUB3.9, Diagnoses and Examinations, MUB3.15, Ab 1D4, NFB01, Allelomorph, 1D4, mAB1D4, FASII, l(1)G0048, MAB1D4, FAS II, FAS 11, Dipteras, FASCIATA 2, fas-II, mAb1D4, clone 1.60, Allele, fasII, l(1)G0081, Fas, Diagnose</description_synonyms></additional><is_claimable>false</is_claimable><name></name><description>Sequencing of flies to diagnose Fas2 allele differences</description><dates><last_updated>2024-03-30</last_updated><first_public>2024-03-30</first_public></dates><accession>PRJNA1081931</accession><cross_references/></HashMap>