JAK, Tum, l(1)hop, DmHD-160, Hopskotch
genotype percent viable ____________________________ hop29/hop25 12% hop3/hop25 16% hop14/hop25 40% hop12/hop25 68% hop27/hop25 100% hop32/hop25 100% hop33/hop25 100%
janus family tyrosine kinase - regulates during segmentation - mutation creates an activated oncogene, causing hematopoietic neoplasms, overproliferation, and premature differentiation.
Gene model reviewed during 5.52
There is only one protein coding transcript and one polypeptide associated with this gene
Forms a complex with Hsp83 and piwi; probably Hop mediates the interaction between piwi and Hsp83.
Possesses two phosphotransferase domains. The second one probably contains the catalytic domain (By similarity), while the presence of slight differences suggest a different role for domain 1 (By similarity).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\hop using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\hop in GBrowse 2
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.
Treatment of S2-derived S2-NP cells with dsRNA made from templates generated with primers directed against hop results in a 12-24-fold decrease in JAK/STAT activity.
When dsRNA constructs are made and transiently transfected into S2 cells in RNAi experiments, an increase in the proportion of G1 phase cells is seen.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Stat92E is part of an intracellular Jak-Stat signalling pathway and is activated by the hop Jak kinase. Partial loss of hop gene product activity gives a phenotype similar to that of Stat92E mutants, supporting the idea that the Jak-Stat pathway is involved in regulation of oogenesis.
hop is required for the renewal of male germline stem cells and for maintenance of the somatic cyst progenitor cell population in the testis.
hop is required for cell proliferation/survival in the eye imaginal disc, for the differentiation of photoreceptor cells, and for the establishment of the equator and of ommatidial polarity.
Candidate gene for testicular atrophy quantitative trait locus.
Phylogenetic analysis of the PTK family.
Mutants display neoplastic phenotype.
Identification: Identified by PCR fragment; relationship to other protein tyrosine kinase genes not known.
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 morphologically normal, but 40% of the homozygous females and 85% of the hemizygous females showing major defects). Heteroallelic females are lethal with the exceptions noted under the alleles. There is a maternal effect on thoracic and abdominal segments, the most extreme embryos <up>produced from homozygous "l(1)hop" germ-line clones that have not received a paternal copy of hop+</up> 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 germ-line 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.
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.