hop32/hop25 mutant flies die more rapidly than do wild-type controls following Drosophila C virus (DCV) infection, and contain about 10-fold more virus.
Compared with wild-type, hop32/hop25 mutant flies show decreased survival and contain significantly more virus particles when injected with Cricket Paralysis Virus (CrPV).
Approximately 68% of adult hemizygous male escapers lose locomotor activity rhythms under constant darkness conditions
Stalks form in early hop3/hop25 egg chambers and the oocyte moves to the posterior of the egg chamber as in wild type. However, the stalk cells fail to intercalate and the stalk consists of two rows of cells linked by adherens junctions. At later stages, the stalks collapse and fusions between egg chambers are seen.
hop32/hop25 flies infected with Drosophila C virus have increased levels of viral RNA and viral capsid proteins than infected wild-type flies. hop32/hop25 flies show reduced survival compared to wild-type flies when injected with a low dose (1 x 102 LD50) of Drosophila C virus.
hop25/hop32 animals have an ectopic vein near the posterior crossvein of the wing.
The mean ln (natural logarithm) circulating hemocyte concentration (CHC) value of hemizygous larvae is significantly higher than that of control siblings. The ability of hemizygous larvae to encapsulate L.boulardi eggs is significantly reduced compared to that of control larvae.
There is no nuclear translocation of Stat92E protein into the nuclei of cells in the fat body in response to challenge with bacteria in hop25/hop32 mutant adult flies.
Embryos derived from mothers carrying hop25 germ-line clones have weak segmentation defects, visible as gaps and malformations of abdominal ventral denticle belts, particularly A4, A5 and A7. Many of these embryos hatch.
hop25/hop2 egg chambers lack border follicle cells and have reduced numbers of stretched (nurse) follicle cells and posterior follicle cells, but increased numbers of main body (oocyte) follicle cells. Nurse follicle cell and centripetally migrating follicle cell domains are shifted posteriorly.
hop25/hop3 mutant females have reduced fertility and fused egg chamber phenotype.
hop25/hop3 ovaries often have compound egg chambers. The chambers contain multiple germline cysts each with its own oocyte and the chambers contain a multiple of 15 ring canals per chamber, indicating that these compound chambers are due to fusion or improper incapsulation of germline cysts rather than extra rounds of germline proliferation. hop25/hop3 egg chambers have extra polar follicle cells. hop25/hop32 females show extensive fusion of egg chambers and stalk cells are rare or absent. hop25/hop33 non-fused egg chambers often have extra polar follicle cells (having 3 or 4 cells rather than the normal number of 2 polar cells at both the anterior and posterior ends of the egg chamber). At stage 8/9, 93% of egg chambers have extra polar cells at the anterior end and 67% of egg chambers have extra polar cells at the posterior end. The number of interfollicular cells is reduced. The extra polar cells do not appear to be due to continued proliferation of the polar cell population. hop25/hop27 non-fused egg chambers sometimes have extra polar follicle cells (generally having 3 rather than the normal number of 2 polar cells at both the anterior and posterior ends of the egg chamber). At stage 8/9, 13% of egg chambers have extra polar cells at the anterior end and 36% of egg chambers have extra polar cells at the posterior end. The extra polar cells do not appear to be due to continued proliferation of the polar cell population. 5% of hop25/hop27 egg chambers are fused.
Adult mutant males lack renewing germ line. The testes are shorter than normal and contain several bundles of elongated spermatids but completely lack early germ cell stages. Mutant embryonic gonads contain the normal number of primordial germ cells. Loss of stem cells is seen in mutant testes by the first larval instar, becoming more apparent in the second larval instar. Single germ cells are not detected at the apical tip of mutant first and second larval instar testes (in contrast to wild type), instead, the testes contain only a few clusters of differentiating germ cells, which resemble spermatogonia or early spermatocytes. 35% of mutant third larval instar testes have no somatic cyst progenitor cells (CPCs). The number of early cyst cells is dramatically reduced in the remaining 65% of testes. Somatic apical hub cells appear normal.
Mutant adult testes contain hub cells but lack stem cells and spermatogonia.
hop25/hop3 females show a mild reduction in eye size and show roughness in the equatorial region, within which ommatidial fusion and duplicated bristles can be seen. hop25/hop32 females can have eyes that are smaller in the dorso-ventral axis with significantly fewer ommatidia compared to wild-type. Ommatidia are arranged irregularly and duplicated bristles are seen. hop25/hop32 females with an eyeless phenotype with a concomitant duplication of the antenna can also be seen. In hop25 homozygotes misrotation and chirality change is seen in the ommatidia. In hop25/hop3 females a loss of photoreceptor cells is seen, misrotations and loss of ommatidial chirality is seen.
Homozygotes show 25% viability. 100% viable in transheterozygous combination with hop27, hop14, hop3 or hop12. 70% viable in transheterozygous combination with hop33, 50% viable in transheterozygous combination with hop32, 5% viable in transheterozygous combination with hopM637 and 2% viable in transheterozygous combination with hop29.
Embryos derived from homozygous mothers show weak segmentation defects. This phenotype is exacerbated by reduction of Stat92E dosage.
Semilethal: 9% of viability.
Homozygous females are less viable than hemizygous males. Hemizygous males have rudimentary testes that do not mature properly and hemizygous or homozygous females have atrophic gonads and no egg chambers are detectable. Germline clone analysis demonstrates that embryos have one abdominal segment missing and A4 appears wider than wild type, and partial or complete fusion of T1 and T2.
The viability and fertility of both male and female flies is adversely affected by this mutation. Hemizygous males have rudimentary testes, which either lack gametes, or contain gametes ranging from early stages to the spermatid stage. Spermatid maturation is abnormal and terminates at an early stage. Axonemes are incomplete or degenerate, and many mitochondrial derivatives are associated with membranes other than the axonemal sheath.
Mutation blocks gene functions that are critical to the development of both reproductive and non-reproductive tissues. Testes devoid of gametes.
viability and fertility poor in males and females. Testes of hemizygous males are usually rudimentary and lack sperm; ovaries of homozygous and hemizygous females usually abnormal, lack egg chambers <up>believed to be somatic defect since eggs appear normal when allele is analyzed in germ-line clones (Perrimon and Mahowald, 1986a)</up>. hop29/hop25 12% viable hop3/hop25 16% viable hop14/hop25 40% viable hop12/hop25 68% viable hop27/hop25 100% viable hop32/hop25 100% viable hop33/hop25 100% viable