(Alliance, FBgn0004864 )

Tyrosine kinase of the non-receptor type, phosphorylates the marelle protein. Required maternally for the establishment of the normal array of embryonic segments: involved in the control of pair-rule gene transcription in a stripe-specific manner. Together with Hsp83 and piwi, mediates canalization, also known as developmental robustness, likely via epigenetic silencing of existing genetic variants and suppression of transposon-induced new genetic variation.

(UniProt, Q24592)

The wild-type allele of hop is required for the continued cell division of all diploid cells as well as the establishment of the normal array of segments. Most of the mutants are homozygous late zygotic (L-P) lethals; one mutant is a larval lethal; two other mutants have some adult survivors (hemizygous males being morphologaically normal, but 40% of the homzygous females and 85% of the hemizygous females showing major defects). Most of the heteroallelic females are lethal, with the following exceptions:

All viable heteroallelic combinations are female sterile, failing to produce eggs or laying abnormal eggs that are small, with a clear chorion and with chorionic filaments absent or partially fused (Perrimon and Mahowald, 1986a). There is a maternal effect on thoracic and abdominal segments, the most extreme embryos [produced from homozygous l(1)hop germline clones that have not received a paternal copy of hop+] showing defects in the posterior spiracles and in segments T2 (denticle belt deleted). T3, A4, and A5 (segment missing) and A8 (segment reduced in size); the least extreme mutant embryos from germline clones show defects in segment A5. Defects visible in early segmentation stages. The extent of the defects is dependent on the strength of the maternal alleles and the paternal contribution. Wild-type sperm can rescue all defects, except those in A5. A few of the rescued progeny hatch and develop into adults.

Dominant tumorous gene that is a temperature-sensitive lethal at 29 in hemizygous males and homozygous females; about two-thirds of the hemizygous males survive at 18 and one-quarter of these have melanotic tumors. Males raised at 26 and heterozygous females raised at 29 survive to adulthood, but show melanotic masses in the abdominal cavity or small black specks in the legs, wings, or thorax. Mutant larvae kept at 29 show enlargement of the lymph glands in the late second- or early third-instar larvae, but no melanotic masses. By mid third-instar, the lymph glands are large and diffuse and the gastric caeca have become encapsulated and melanized. By late third-instar, the larvae have melanotic masses in the body cavity, lack lymph glands, and have reduced, encapsulated and melanized gastric caeca as well as encapsulated and melanized muscles and fat bodies. These mutants do not survive beyond the late third-instar or the early pupal stage. When lymph glands from Tum larvae are injected into adult female hosts, transplantable neoplasms are produced. Melanization, at first associated with the leg joints and later with the head, thorax, and abdomen, takes place; also abdominal bloating. The lymph glands become melanotic and the abdomen is filled with encapsulated masses before the premature death of the injected individuals. Injection of Tum tissue other than lymph glands fails to produce these effects. The melanotic neoplasms can be transplanted into a succession of hosts in which they produce the same abnormalities. The neoplastic cells resemble hemocytes; some cell lines are melanotic and others are unpigmented, but in both types, the tissue, when transplanted, grows rapidly in the hosts and kills them.