wing cell & wing vein L3 & wing vein L4 | somatic clone
Only a few knKN4 homozygous mutants survive to late embryonic stages.
The dendritic arbors of single class IV da neurons homozygous for knKN4 (generated by the MARCM system) are less elaborate and show decreased size compared with wild-type.
Homozygous small clones (induced in the mid-third larval instar stage) result in ectopic vein material in the wing only if the clones are located between wing veins 3 and 4. The ectopic vein material often extends outside the clone, indicating non-autonomy.
Homozygous knKN4 larvae consistently exhibit head defects. They lack ventral arms and have foreshortened lateralgrate. The hypopharyngeal lobe is also missing in these larvae.
Embryonic segmentation is normal. Transheterozygotes with kn1 enhance the kn1 wing vein phenotype, the veins are extensively fused. This loss of intervein region reduced the length and width of the wings by 80-90%. The transition point between socketed and unsocketed bristles at the wing margin is shifted posteriorly to the shifted position of wing vein L3. Germline clones give rise to fully viable offspring when outcrossed to kn+ sperm and does not alter the larval lethality when fertilised with knKN1, knKN2, knKN3 or knKN4 sperm. Clones generated in adult cuticle are normal unless induced in the anterior compartment of the wing in the intervein region between veins L3 and L4. Clones obey the A-P compartment boundary but when they are induced along the boundary the result is an ectopic or shifted vein with an associated loss of vein L4 in the non-mutant posterior compartment. Clones located at the wing margin generated terminal vein 3 bristles rather than true marginal bristles.
knKN4 is a suppressor of wing vein L2 phenotype of ptcG20
Doubly mutant mosaic clones with ptcS2 are very similar to clones mutant for ptcS2 alone that affect global organisation: reorganisation of the wing when induced in the anterior compartment and clones induced near the anterior margin induce a complete duplication of the anterior wing blade. The kn mutant affects local alteration in wing patterning associated with ptc inactivation. Loss of wing vein L2 in ptcG20 mutants is suppressed when simultaneously mutant for kn.