FB2020_06, released Dec 22, 2020
Gene: Dmel\ea
FB2020_06, released Dec 22, 2020
Gene: Dmel\ea
Gene: Dmel\ea
Gene: Dmel\ea
required for establishment of embryonic polarity - secreted serine protease, trypsin family - generates processed Späzle, which in turn acts as the Toll ligand - restricted to the dorso-ventral patterning of the embryo
Please see the JBrowse view of Dmel\ea for information on other features
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Gene model reviewed during 5.47
Low-frequency RNA-Seq exon junction(s) not annotated.
1.5 (northern blot)
None of the polypeptides share 100% sequence identity.
392 (aa); 43 (kD predicted)
Activation peptide and active catalytic domain are associated by a disulfide bond. Processed easter is present in extremely low amounts in the early embryo as it is rapidly converted into a high molecular mass complex, which may contain a protease inhibitor. Zymogen activation is also controlled by a negative feedback loop from Dorsal.
The clip domain consists of 35-55 residues which are 'knitted' together usually by 3 conserved disulfide bonds forming a clip-like compact structure.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ea using the Feature Mapper tool.
Comment: maternally deposited
ea transcripts are expressed in ovaries and in early embryos.
Comment: paper states 0-3 hr AEL
ea protein is uniformly distributed in the blastoderm embryo.
GBrowse - Visual display of RNA-Seq signals
View Dmel\ea in GBrowse 23-57
3-56.1
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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.
polyclonal
Shows particularly robust cycling of transcription in adult heads, as assessed by expression analysis using high density oligonucleotide arrays with probe generated during three 12-point time course experiments over the course of 6 days. Shows significant change of expression pattern in circadian mutant background; decreased expression in per01, tim01 and ClkJrk background.
ea can directly cleave spz at a unique position, the spz carboxy-terminal fragment generated has the biological and biochemical properties of the polarising activity of spz, it exists as a disulfide-linked dimer and appears to share structural similarities with the nerve growth factor and the neurotrophin family of growth factor ligands.
ea is not required for muscle development in the embryo.
The zymogen form of ea is processed in vivo by a proteolytic cleavage event that requires three upstream proteases. Processed ea is present in extremely low amounts in the early embryo because it is rapidly converted into a high molecular mass complex, which may contain a protease inhibitor. ea zymogen activation is also controlled by a negative feedback loop from dl.
Spatial regulation of ea activity by localized zymogen activation is a key initial event in defining the polarity of the dorsal-ventral embryonic pattern.
Protein shows similarity with proclotting enzyme light chain of Tachypleus: S-S linking of ea protein predicted.
In the absence of ea activity in the perivitelline fluid no Tl ligand is detected suggesting that ea activity is involved in the production of the Tl ligand.
Mutations in maternal dorsal class gene ea do not interact with RpII140wimp.
Analysis of mosaic females indicates that Ser, ea, snk and tub are expressed in the germline during oogenesis.
Involved in the regulatory hierarchy responsible for the asymmetric distribution and function of zygotic regulatory gene products along the DV axis of early embryos.
Maternal effect lethal; both recessive loss-of-function and dominant gain-of-function (eaD) alleles female sterile. Embryos produced by females homozygous for recessive alleles are dorsalized; lack ventral and lateral elements similar to embryos produced by dl/dl females; dorsal folds extend around circumference of embryo; lateral head fold and ventral furrow fail to form; germ band does not extend and cuticle forms a tube with dorsal characteristics throughout. Degree of dorsalization proportional to level of ea expression as demonstrated by hypomorphic and temperature-sensitive alleles. Temperature sensitive period as demonstrated by ea14 from the time of pole-cell formation to gastrulation; developmental Northern blots demonstrate the presence of transcript in the ovaries and increased levels during the first four hours of embryonic development followed by a marked decline between hours four and six. Partial rescue of mutant phenotype achieved by injection of cytoplasm or poly(A)+ RNA from wild-type embryos or embryos from females homozygous for other dorsal-group mutants; spatial source of donor cytoplasm unimportant; degree of rescue reduced with distance from site of injection; complete rescue producing viable and fertile adults achievable with injection of purified ea+ mRNA. tw, a zygotically active member of the dorsal group of genes, is not expressed in such embryos (Thisse, Stoetzel, El Messal and Perrin-Schmidt, 1987); furthermore strong alleles allow zen expression ventrally where it is not normally observed (Rushlow, Frasch, Doyle and Levine, 1987); periodicity of ftz stripes slightly disrupted in embryos from ea mothers (Carroll, Winslow, Twombly and Scott, 1987). Females heterozygous for fully penetrant dominant alleles are sterile; the offspring of eaD3/+ females display ventralization or lateralization as indicated by lateral extension of the denticle bands; patches or rings of denticles may encircle the embryo; however, the mesoderm, the most ventral pattern element, is not increased; dorsal structures such as filzkorper, antennal and maxillary sense organs are absent; field of dorsal hairs greatly reduced. eaD2/+ females are lateralized, producing embryos that lack presumptive mesoderm and have no ventral furrow, show dorsoventrally symmetrical folding at gastrulation with the lateral head fold encircling the embryo and do not undergo germ band extension. Injection of ea-deficient embryos with 200 times the quantity of mRNA required for complete rescue does not cause ventralization, indicating that gain of function alleles are not merely hypomorphic in nature.
