The concentration of circulating hemocytes in Egfrf24 heterozygous third instar larvae is comparable to that in wild-type controls.
Df(2R)Egfr3/Egfrf24 mutant embryos exhibit severe defects in ventral patterning. The embryos are very short with no denticle belts and a large anterior hole.
Egfrf24 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 Egfrf24 mutant terminal cells exhibit defective lumen.
Although the initial growth of Egfrf24 mutant intestinal stem cell clones is normal, their long-term proliferation is severely compromised. These clones do not grow even after the flies have recovered from Pseudomonas entomophila infection.
In contrast to wild-type, supplementing Apis mellifera royal jelly to food does not influence body size or developmental time in Egfrtsla/Egfrf24 mutants. When wild-type flies are reared on medium containing royal jelly, they show increased body size (body weight and body length) and fecundity, and have extended lifespan and shortened developmental time compared with flies reared on control medium.
In stage 16 Egfrtsla/Egfrf24 embryos the two neurons that normally arise closest to the midline are lost, vdaB (in 79% of cases) and the class III neurons (in 76% of cases). Loss of these neurons are preceded by the loss of SOPs 1a (73%() and 1 (69%).
Egfrf24/EgfrT1 flies have severe rough eyes which have a reduced number of photoreceptor cells per ommatidium. Most of vein L4 is lost in the wing.
The cardiac function of Egfrf24/Egfrtsla flies is similar to that of wild-type controls at 18[o]C. The cardiac function of Egfrf24/Egfrtsla flies deteriorates after 24 h at 25[o]C.
Marker expression analysis shows that in Egfrtsla/Egfrf24 flies heat shocked for 24 hours at the beginning of pupariation, the proportion of pale-ommatidia is reduced and hybrid ommatidia are present with a yellow-type R8 and a pale-type R7. These animals have very rough eyes.
Homozygous Egfrf24 mutant adult midgut progenitor cells fail to proliferate during larval development.
Egfrf24/+ flies show rotation defects in 26% of ommatidia.
Primordial germ cells overproliferate in Egfrtsla/Egfrf24 larvae grown at a restrictive temperature. Fewer intermingled cells (somatic cells adjacent to primordial germ cells) are present in Egfrtsla/Egfrf24 gonads compared to wild-type.
Oocyte polarity is disrupted when the posterior follicle cell layer contains Egfrf24 mutant clones.
Egfrt1/Egfrf24 animals show loss of the anterior crossvein (100% penetrance) and partial loss of vein L4 in the wing (169% penetrance).
Egfrtsla/Egfrf24 animals shifted to restrictive temperatures for 24 hours during the first half of the third larval instar have leg truncations, with the size of the truncation increasing with temperature. At lower restrictive temperatures (28.7oC) only the most distal structures (the claws) are missing but at high temperatures (33oC) structures tarsal segments 2-5 are absent. At 33oC development of regions more proximal to the tarsal segments is occasionally disrupted. Egfrtsla/Egfrf24 clones do not survive in distal regions of the leg disc at temperatures above 31oC. Egfrtsla/Egfrf24 animals shifted to 33oC for 12 hours during the first quarter of the third larval instar show truncations of the tarsus. However, a 12 hour shift during the second quarter of the third larval instar results in legs with normal distal elements (claw and tarsal segment 5) but fusions or deletions of the intermediate tarsal segments 2-4.
When Egfrtsla/Egfrf24 mutants are grown at the permissive temperature (18oC) throughout larval development, and then shifted to the non-permissive temperature (29oC) between 0 and 10 hours after puparium formation (APF) recognizable transverse rows (t-rows) of bristles are seen on the basitarsus and distal tibia are seen, but bristles within each row are jumbled in irregular groups. (bristles line up, with sockets touching in wild-type). Up shifts after 10h APF have little effect. When these mutants are grown at 18oC throughout larval development, shifted up to 29oCat pupariation and shifted back down between 0 and 14 hours APF, little effect is seen. Down shifts after 21h APF cause disruption of the organisation of the t-rows. When downshifts occur between 14 and 20h APF, other phenotypes emerge. In a minority of legs (13%) adjacent rows bend toward one another and join at Y or X shaped intersections.
When Egfrtsla/Egfrf24 animals are raised at the permissive temperature (of 18oC) they have a wild-type pattern of bracts. Those raised at 29oC lack all bracts. The sensitive period for tibial and basitarsal bracts are 17-28h and 13-28h AP respectively.
Only 2% of egg chambers contain homozygous follicle cell clones 5 days after clone induction. Homozygous follicle cell clones are detected 3 days after clone induction, but they are smaller and less frequent than control clones.
In Egfrf24 embryos division cycles 14 to 16 in the Malpighian tubules occur normally. But arrest occurs from Cycle 17. The number of Malpighian tubule is about 39 after 8 hours, but is eventually reduced to about about 26 by cell death (wild type Malpighian tubules have about 125 cells).
Homozygous clones in the eye disc lack mitosis completely. Posterior to the morphogenetic furrow, mutant clones undergo S phase, as shown by BrdU incorporation.
Egfrtsla/Egfrf24 flies at 18oC frequently lack the anterior supraalar bristle, posterior supraalar bristle and posterior postalar bristle, and the anterior postalar bristle and anterior dorsocentral bristle are frequently duplicated. When late LIII larvae are shifted to 30oC for 15 hours, all notum macrochaetae show reduced liklihood to develop except the scutellar bristles.
When all outer border cells are mutant for Egfrf24 in egg chambers containing homozygous clones, the cluster remains in the centre of the egg chamber at stage 10, whereas 90% of wild-type clusters are found dorsally. When mixed clusters with both wild-type and mutant cells move dorsally, the wild-type cells are in front. When patches of border cells are mutant for Egfrf24 in egg chambers containing homozygous clones, the border cells still migrate dorsally.
Egfrf24/Egfrtsla embryos raised at 18oC until approximately stage 12, and then shifted to 29oC for the remainder of development exhibit reduced numbers and increased apoptosis of longitudinal (interface) glial cells.
Egfrf24/Egfrtsla animals kept at the restrictive temperature between 168-180 hours after egg deposition (AED) develop an adult eye that lacks ommatidia. Imaginal discs from these animals examined at either 192 or 204 hours AED lack both the ommatidia and the morphogenetic furrow. Egfrf24/Egfrtsla animals kept at the restrictive temperature between 192-204 hours AED develop an eye with severe structural defects along the posterior-lateral margins (ommatidia at the intersection of the equator and posterior margin appear not to be affected). The morphogenetic furrow has clearly initiated at the posterior margin in imaginal discs from these animals examined at 204 hours AED, but its continued re-initiation along the lateral margins is inhibited.
If Egfrtsla/Egfrf24 flies are raised at 17oC, transferred to 25oC for 24 hours at second instar larval stages, and then returned to 17oC leads to a mirror image duplication of the wing.
When Egfrtsla/Egfrf24 mutant males are raised at the permissive temperature (18oC), and then shifted to the restrictive temperature (29oC), a spermatogenesis phenotype is seen. Although all stages of spermatogenesis are initially present, by one week of at non-permissive temperature, testes are filled with massive numbers of early germ cells with small nuclei. The early germ cells appear to proliferate at the expense of differentiation, as spermatocytes and spermatids are absent or markedly reduced in numbers. Many early germ cells displayed expression marker, subcellular structures and cell division behaviour characteristic of stem cells and gonialblasts. Mutants have many more cells with ball shaped or dumbbell-shaped spectrosomes, both near the tip and displaced down the testis. In Egfrtsla/Egfrf24 mutant males, early cyst cells often form improper associations with early germ cells. In general accumulation of early germ cells is not associated with a corresponding increase in the total number of cyst progenitor or early cyst cells. Homozygous Egfrf24 germline clones produce cysts with the normal number of differentiating spermatocytes. No overproliferation of early germ cells is seen.
When Egfrtsla/Egfrf24 flies are grown at the restrictive temperature for Egfrtsla during the second instar, the notum is lost, the wings are present but have pattern abnormalities and fail to inflate.
Suppresses the dominant EgfrE1 phenotype towards wild-type in transheterozygotes.
Homozygotes have mutant egg chambers.
orbF343 interact genetically with Egfr, double heterozygote embryos display fused dorsal appendages.
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.
Homozygous embryos fail to complete germ band retraction, lack most anterior, posterior and ventral cuticle, and have reduced or no denticles. Cell death is seen in the head, amnioserosa and germband at stage 10, and abnormally deep segmental grooves are seen on the outside of the germband. By stage 12, large patches of dead cells are seen in the amnioserosa, the brain and cephalic epidermis, and clumps of necrotic cells appear in what may be a segmentally repeated pattern in the epidermal tissues of the germ band.
The viability of homozygous clones in the wing is very low. Homozygous clones in the legs, notum and head seem to be inviable. Homozygous clones in the abdominal tergites are viable. Wild-type chaetae are clustered immediately adjacent to or included within these clones and there is a depletion of chaetae around the clones for several cell diameters.
Severe 'flb' phenotype. Embryos produced from heteroallelic combination with Egfrt1 have a severe ventralised phenotype, reduction in size of their dorsal appendage.
Embryonic head appears to be abnormal at the time of stomodeal invagination: clumps of cells fall away.