Open Close
General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
col1, kncol1
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Nucleotide substitution: G to A. The mutation at amino acid position 228 eliminates a splice acceptor site, which should result in the non-removal of intron 6 and the production of a truncated protein.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

In kncol-1/kncol-3 embryos ap-expressing neurons fail to project their axons into the medial-most Fas2-immunopositive fascicle in the ventral nerve cord. Their commissural (but not lateral) projections are also impaired.

kncol-1 kn+m5 larvae show melanisation of crystal cells after heating at 65[o]C for 10 minutes, as occurs in wild-type larvae.

kncol-1 mutant larvae have no prohemocytes.

Homozygous embryos show a transformation of muscle DA3 to DA2 morphology.

All dorso-lateral muscles are either missing or mis-specified in kncol-1 embryos, while the more dorsal or more ventral muscles are not affected. The most frequently observed defects are DA3>DA2, LL1>DA3 and DO4>DO5 transformations, which indicate changes in progenitor identity. Many myofibres are mis-orientated.

40% of segments in kncol85-GAL4/kncol-1 embryos show a complete DA3>DA2 morphological transformation. In most other segments, the DA3>DA2 muscle maintains thin projections toward the wild type DA3 attachment site, suggesting an incomplete transformation.

kncol-1 mutant embryos have a significant reduction in the number of even-skipped (eve)-expressing neurons in the EL cluster by stage 15, but no difference in the number of other eve-expressing neurons (aCC, RP2, pCC and U/CQ), compared to wild-type controls.

The number of SE2 neurons is normal in kncol-1/kncol-3 mutant animals.

BrdU incorporation in the lymph gland is increased relative to wild-type in mutant third instar larvae and the incorporation becomes distributed throughout the lymph gland. Differentiated cells are found throughout the lymph gland lobe, in contrast to wild type, where they are restricted to the peripheral cortical zone.

In kncol-1 homozygotes and kncol-1/Df(2R)AN293 mutant animals rescued to adult viability by kn+m5 do have plasmatocytes and crystal cells as normal, however when exposed to wasp parasitization a complete lack of lamellocytes is seen (in contrast to the increased numbers seen in wild-type).

Wings veins L3 and L4 are closer to each other in kncol-1/kn1 animals than in wild type and are apposed proximally. The L3-L4 intervein is 66+/-6% smaller than wild type, whereas the anterior margin to L2 and L2-L3 interveins are normal in size. The L4-L5 and L5 to posterior margin interveins are smaller than wild type. The wave of mitosis that normally takes place in each intervein primordium between 15 and 21 hours after puparium formation is specifically absent from the central region of kncol-1/kn1 wings. kncol-1 homozygotes (rescued to adult viability by kn+m5) lack the L3-L4 intervein in the wing. A central larger L3-type vein is present in these flies and only a small, proximal region of wing vein L4 forms. There is a 20% overall reduction in wing size compared to wild type. The L2-L3 intervein is 12+/-5% larger than in wild type. The L4-L5 and L5 to posterior margin interveins are smaller than wild type. The wave of mitosis that normally takes place in each intervein primordium between 15 and 21 hours after puparium formation is specifically absent from the central region of the wings of kncol-1 animals rescued with kn+m5. Loss of wing vein L4 is seen in wings containing homozygous kncol-1 clones that encompass most, if not all, dorsal and ventral cells in the L3-L4 region. Wing vein L4 does form when homozygous dorsal and ventral cells span 3-4 rows of cells along the anterior posterior boundary.

Muscle DA3A/DA4T is missing or (in a few cases) reduced to a thinned muscle. This phenotype is highly penetrant and specific.

Lethality occurs during the late embryonic to first larval instar stage. Homozygous and hemizygous embryos have head defects; the ventral arms are missing and the lateralgraten are reduced. The T-ribs in the floor of the pharynx, and the antennal, maxillary or hypopharyngeal sensory organs are present and a normal pattern of internal sensory structures is seen. The embryos that hatch do not grow and tend to crawl out of the medium, suggesting that they are unable to feed.

Homozygotes and hemizygotes die as embryos or larvae. In a kn1/kncol-1 transheterozygote, the proximal regions of wing veins L3 and L4 are apposed, and the anterior crossvein is missing. When kn+m5 is used to partially rescue the homozygous kncol-1 phenotype, a wing vein phenotype remains. The L3-L4 intervein or anterior crossvein is completely absent, the overall size of the wing and the number of innervated bristles at the anterior margin are unchanged. Wing veins L3 and L4 are apposed and abnormally large, each vein maintaining its identity. The number, ratio and position along the A-P axis of socketed and unsocketed bristles is normal.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by

kn1/kncol-1 has visible phenotype, enhanceable by hhts2

Suppressor of
Phenotype Manifest In
Enhanced by

kn1/kncol-1 has wing vein phenotype, enhanceable by hhts2

kn1/kncol-1 has wing vein L3 phenotype, enhanceable by hhts2

kn1/kncol-1 has wing vein L4 phenotype, enhanceable by hhts2

kncol-1 has wing vein L3 phenotype, enhanceable by fu[+]/fu1

kncol-1 has wing vein L4 phenotype, enhanceable by fu[+]/fu1

Suppressed by
NOT suppressed by
Enhancer of

kn[+]/kncol-1 is an enhancer of wing vein L3 phenotype of fu1

kn[+]/kncol-1 is an enhancer of wing vein L4 phenotype of fu1

Suppressor of
Additional Comments
Genetic Interactions

Overexpression of asrijScer\UAS.cKa in kncol-1 larval lymph glands under the control of Scer\GAL4e33C can suppress the prohemocyte-phenotype.

tupex4 kncol-1 double mutant embryos show a cumulative phenotype with respect to the somatic muscle, showing dorsal muscle defects and a lack of DA3 muscle.

Expression of vnScer\UAS.cSa under the control of Scer\GAL4dpp.blk1 does not rescue wing vein L4 formation in kncol-1 animals rescued with kn+m5, while the larger L3-type vein seen in these animals is widened.

Crossing kncol-1 with hhScer\UAS.cCa, driven by Scer\GAL4en-e16E suppresses the wing vein phenotype caused by ectopic expression of hhScer\UAS.cCa. kncol-1 restores the presence of an almost wild type position of wing vein L3 and its associated sensillae. An ectopic crossvein can be seen in the L2-L3 intervein. In fu1 and kncol-1 double heterozygotes, wing veins L3 and L4 are fused for most of their lengths. This is an enhancement of the phenotype of either mutation alone. At 25oC hhts2 enhances the wing vein phenotype seen in kncol-1/kn1.

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by

kncol-1 is partially rescued by kn+m5


The combination of kncol-1 and kn lethal mutations results in embryonic lethality.

Images (0)
Stocks (2)
Notes on Origin
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (27)