FlyBase: updates to theDrosophila melanogasterknowledge base

Abstract

FlyBase (flybase.org) is an essential online database for researchers using Drosophila melanogaster as a model organism, facilitating access to a diverse array of information that includes genetic, molecular, genomic and reagent resources. Here, we describe the introduction of several new features at FlyBase, including Pathway Reports, paralog information, disease models based on orthology, customizable tables within reports and overview displays (‘ribbons’) of expression and disease data. We also describe a variety of recent important updates, including incorporation of a developmental proteome, upgrades to the GAL4 search tab, additional Experimental Tool Reports, migration to JBrowse for genome browsing and improvements to batch queries/downloads and the Fast-Track Your Paper tool.

Chromatin and transcriptomic profiling uncover dysregulation of the Tip60 HAT/HDAC2 epigenomic landscape in the neurodegenerative brain

“…6). These genes regulate roles in synaptic plasticity and neuronal developmental processes that include synaptic vesicle function (Syn & nwk), axonal outgrowth (NetB), neuronal signaling pathways (nmo, flw, Dop1R1, Dl, Appl, & RhoGAP100F), gene regulation (trx & Thor), actin filament formation and stabilization (Shroom), and neurodevelopment process (oc) (Larkin et al, 2020). Tip60 and HDAC2 not only both bind within each of these genes in all fly genotypes analyzed (APP, APP;Tip60, w 1118 ) but remarkably, at almost identical genomic coordinates, suggesting that Tip60 and HDAC2 are co-recruited to the same docking sites within gene loci.…”

Alzheimer’s disease-associatedTM2Dgenes regulate Notch signaling and neuronal function inDrosophila

“…The neurogenic defect is a classical phenotype in Drosophila that was originally reported in the mid-1930s (Artavanis-Tsakonas andMuskavitch, 2010;Yamamoto et al, 2014), and the study of mutants that show this phenotype led to the establishment of the core Notch signaling pathway in the late 1980's and early 1990's (Artavanis-Tsakonas et al, 1995;Lehmann et al, 1981). Although the study of neurogenic phenotypes and genes has a long history, this phenotype is a very rare defect that has so far been associated with only 18 genes according to FlyBase (Larkin et al, 2021), prior to this work. Seven genes show this defect as zygotic mutants [aqz, bib, Dl, E(spl)m8-HLH, mam, N and neur], seven genes are zygotically-required essential genes with large maternal contributions (hence the need to generate maternal-zygotic mutants by generating germline clones to reveal the embryonic neurogenic defect) [Gmd, Gmer, gro, Nct, O-fut1, Psn and Su(H)], one gene has only been investigated by RNAi (Par-1) and four genes including amx are non-essential genes and show maternal-effect neurogenic defects (amx, brn, egh, pcx).…”

Combined Transcriptomic and Proteomic Analysis of Perk Toxicity Pathways

“…We used the full list of Drosophila uORFs from a recent study by Zhang and colleagues [ 69 ]. Briefly, they queried all Drosophila genes from the FlyBase database [ 79 ] and identified 7036 genes with at least 1 uORF, according to their definition (starting with AUG and ending with a stop codon UAA/UAG/UGA). Based on this list, we identified genes that contain uORFs in our total set of genes, group 1 and group 2.…”