AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.52
874 (aa); 125 (kD observed); 98 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\egl using the Feature Mapper tool.
egl RNA is enriched in single cells when the 16-cell cyst forms in region 2A of the germarium. Between stages S2 and S7, egl RNA is concentrated at the posterior cortex of the oocyte. As the oocyte starts to accumulate yolk, egl transcripts localize to an anterior ring at the nurse cell-oocyte boundary. By stage S10, they are distributed evenly throughout the oocyte and persist in the oocyte until early embryogenesis.
The BicD and egl proteins, as previously described for the orb protein, accumulate in the presumptive oocyte following fusome disassembly in germarium region 2a during oocyte specification and are relocalized to the posterior of the oocyte between germarium regions 2b and 3 during oocyte polarization.
egl protein is first detected in the germarium and is evenly distributed in the newly formed 16-cell cyst. By stage S1 of oogenesis, it localizes to a single cell, the future oocyte. From stages S2 to S7 egl protein is enriched at the posterior cortex of the oocyte, wherever the oocyte abuts the follicle cells. At stage S8, it shifts to the anterior cortex in a ring around the margin of the oocyte where the oocyte, nurse cells, and follicle cells meet. Staining is particularly pronounced around the oocyte nucleus. No protein is detec ed in the oocyte after stage S10. egl protein distribution in oocytes closely resembles the distribution of the minus end of microtubules. It was shown that disrupting microtubule organization abolishes egl protein localization. In addition, egl protein and BcD protein were found to have identical distributions during all stages of oogenesis. Localization of egl protein depends on BicD protein and vice versa.
GBrowse - Visual display of RNA-Seq signalsView Dmel\egl in GBrowse 2
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Source for identity of: egl CG4051
Despite lacking a canonical RNA-binding motif, egl protein directly recognises active mRNA localisation elements.
egl promotes the initiation of rapid minus-end directed movement of mRNAs along microtubules.
All of the cells in the female germline cyst form synaptonemal complex in egl mutants.
egl protein colocalises with BicD protein to the oocyte in three stages that correlate with the stepwise polarization of the oocyte. Immunoprecipitation experiments show that both proteins are part of a protein complex. Results propose that the egl-BicD protein complex links microtubule polarity and RNA transport.
Oocyte determination requires egl function in the germ line, but not in the surrounding follicle cells. During early oogenesis the egl-BicD protein complex is required to transport factors promoting oocyte differentiation; during later stages the complex directs the sorting of RNA molecules required for anterior-posterior and dorsoventral patterning of the embryo.
The egl locus is responsible for two functions in cell fate choice in oogenesis: early on it is necessary for inhibition of meiotic entry in the "obligate" pro-nurse cells; later it is necessary for meiotic maintenance in the "winning" pro-oocyte. Both roles can be attributed to a single function by invoking gradients through the early cyst; the egl+ function appears to be required for the normal function of these gradients.
egl mutants have disrupted microtubule cytoskeletons and fail to differentiate an oocyte.
Recessive mutations at egl and BicD, and microtubule assembly inhibitors, disrupt the formation and maintenance of the single polarized microtubule cytoskeleton that connects the oocyte to the 15 nurse cells at the time the oocyte is determined.
egl is required for oogenesis and the determination of polarity within the embryo.