Egfrf2 mutant embryos show severe cardioblast (CB) patterning defects, as well as a lower generic CBs:ostial CBs ratio than the typical 4:2 ratio.
Egfrf2 heterozygous embryos exhibit severe defects in morphogenesis. More than 95% of embryos exhibit a 'faint little ball' phenotype, with the posterior end of the embryo in close proximity to the head, indicating a defect in germband retraction. In less severely 'curled' embryos, holes are visible in the dorsal surface, that typically extend anteriorly into the head.
Prior to the initiation of germband retraction, the amnioserosa of Egfrf2 mutants begins to degrade, which in the most severe cases can lead to a complete and dramatic loss of the tissue. In some embryos the amnioserosa persists throughout germband retraction and dorsal closure, but has noticeably fewer cells than wild-type. Germband retraction appears abnormal in these mutants, as does the amnioserosa, with the tissue constricting perpendicularly to the normal anterior-posterior direction.
Egfrf2 mutants exhibit defects in terminal cell lumenogenesis, with terminal cells lacking a visible gas-filled lumen and exhibiting some branching defects. Only a small percentage (approximately 15%) of Egfrf2 mutant terminal cells exhibit defective lumen.
Blood cell progenitors, nephrocytes and cardioblasts are virtually absent in mutant embryos. Significant amounts of apoptotic cell death occur in the cardiogenic mesoderm of stage 11/12 mutant embryos.
Multiple photoreceptor-R8 cells are not observed in eye tissue from Egfrf2/+ animals.
Mutant stage 9 embryos show neuroblast hypoplasia and reduced mitotic activity in the developing neuroectoderm.
Egfrf2 mutant embryos exhibit a strong tracheal invagination phenotype, where the tight accumulation of actin around the invagination edge is disrupted.
Egfrf2 Minute clones in the eye disc fail to form the arcs and rosettes of cells in the morphogenetic furrow that are seen in wild-type eye discs.
The tracheal system of Egfrf2 embryos show branch interruptions and branches with cells only connected by cytoplasmic extensions.
Egfrf2 homozygous clones in the dorsal air sac primordium grow more slowly than wild-type clones, and are found at the tip of this primordium at a significantly lower frequency than wild-type clones.
No posterior spiracles are present in Egfrf2 larvae.
Egfrf2 clones generated in the wing, using the MARCM technique, that encompass a portion of the posterior crossvein (PCV) and a large portion of the adjacent fifth longitudinal vein cause disruption of the longitudinal vein and the posterior half of the PCV. Residual PCV development can be observed outside of the clone, nearest to the remaining longitudinal veins.
In stage 16 Egfract.B.Scer\UAS; Scer\GAL4en-e16E embryos, there are increased numbers of oenocytes per cluster. The number of oenocytes per cluster follows a multi-modal distribution, with peaks corresponding to multiples of 3 (12, 15, 18 and 21) suggesting that additional rounds of delamination, generally of 3 oeoncytes per round as in wild-type, are occurring. This multi-modal distribution and increased numbers of per cluster are partially suppressed by Egfrf2/+.
Egfrf2 embryos show a disorganization of and a significant loss of lateral ventral cluster sensory neurons in all hemisegments.
Heterozygous females lay eggs with fused or partially fused dorsal appendages (27.8% at 18oC, 24.6% at 25oC and 51.4% at 29oC).
In mutants the hindgut tube is much shortened due to a reduction of the cell number.
Homozygous mutant clones in the adult abdomen alter the distribution of bristles, but the polarity is normal.
Egfrf2 clones induced in the wing disc in a Minute background during the first or early second instar contribute only to the prospective wing blade, while clones induced in the Minute background during the late second and early third instar can also contribute to the wing hinge and medial notum. Egfrf2 clones are not found in the prospective lateral notum. Homozygous clones generated before the second larval instar (before dorsoventral compartmental segregation has occurred) show an extreme preference for the ventral compartment of the wing disc. Homozygous clones generated after dorsoventral compartmental segregation has occurred are restricted to either the dorsal or ventral compartment of the wing disc and survive equally well in either compartment. In rare cases dorsally situated clones in the wing disc from an ectopic ventral compartment.
Intermediate neuroblasts do not form in mutant embryos and medial and lateral neuroblasts lie next to each other.
Within homozygous somatic clones, the spacing of photoreceptor cell R8 cells is irregular. R8 cells usually form several cells away from their neighbours. The R8 cells are less apically restricted than wild type R8 cells.
Egfrf2 embryos have an average of 3.03 +/- 0.03 neurons per lch5 organ.
Heterozygotes show a quantitative effect on wing shape in intervein regions B and C compared to wild type.
Homozygous clones in the eye disc have contain excess R8 cell precursors which are in a less organised pattern than in wild-type discs. Excess cell death is associated with the clones, predominantly posterior to the morphogenetic furrow. Homozygous clones that extend to the margin of the eye disc cause impaired disc growth and excess cell death.
Homozygous embryos have a reduced number of cells in both the anterior and posterior Malpighian tubules compared to wild-type embryos. No BrdU incorporation occurs in the outbudding tubules at a time when cells divide in wild-type embryos.
All RP2 and RP2sib neurons are missing. Intermediate neuroblast column does not form. The development of neuroblast 2-5 is unaffected, neuroblast 1-1 is consistently mis-specified at a low frequency and the intermediate neuroblast 3-2 is absent. Neuroblast 5-2 and 7-1 are affected, with medial 7-1 acquiring characteristics of its lateral neighbor. A significant fraction of medial neuroblasts fail to activate their appropriate gene expression profile. The medial MP2 neuroblast is often incorrectly specified: 50% acquire traits characteristic of other neuroblasts.
The eg/en positive NB 7-3 cluster is missing in most hemineuromeres. In 10% of hemineuromeres neuroblast NB1-1 or NB7-1 are missing. In 97% of hemineuromeres the RP2/RP2sib neuroblasts are missing. GMC4-2a is also missing at earlier stages. 56% of hemineuromeres lack NB7-3. Cells from Egfrf2 mutant embryos have been used to demonstrate that Egfr is cell-autonomously required for the formation of intermediate NB lineages, is dispensable for the formation of lateral NB lineages, and is required for heterotopically transplanted dorsal NE cells to assume ventral NB identities, though not for assuming midline fate.
Germline clones reveal no requirement for Egfr in the oocyte in patterning the egg, or in the viability or patterning of the embryo.
Transheterozygous females with Egfrt1 or Egfrt2 display egg chambers with gaps in the follicular epithelium that uncover the nurse cells. Eggs derived from these females display weak or intermediate ventralised phenotypes.
Enhances the female sterility and adult morphological defects of Egfrt1. Rarely survives as transheterozygote with the semi-viable Egfrtop-CA allele.
Malpighian tubules in homozygous embryos are four tiny outpushings of the posterior hindgut. Reduction in size of the tubules is due to reduction in cell number, not cell death.
No changes in phenotype of tor13D embryos.
Homozygotes and hemizygotes display a severe 'flb' phenotype. Embryos produced from heteroallelic combination with Egfrt1 have a severe ventralised phenotype, reduction in size of their dorsal appendage.