Amino acid replacement: ?88term.
The encoded protein contains only 10% of the normal amino acid sequence.
Nucleotide substitution: G790A.
Amino acid replacement: W87term.
G7308732A
G790A
W87term | brk-PA
?88term
TGG to TAG nonsense mutation in codon Trp87.
Flies bearing brkM68 somatic clones display wing notches and swirled hair in the vicinity of the notches but only occasionally wing outgrowths.
The boundary between the maxillary and mandibular segments is unaffected in brkM68 embryos.
Eggs from females carrying large homozygous somatic follicle cell clones completely lack dorsal appendages.
Somatic clones in the follicle cells of the egg chamber result in eggs with an enlarged operculum and reduced dorsal appendages.
Ectopic veins form along the inner edges of somatic clones of brkM68 homozygous cells located in positions posterior to wing vein L5. When such clones are located anterior to L2 ectopic vein is also induced along the boundary, but both inside and outside the clone. Ectopic venation is not associated with clones found elsewhere in the disc.
brkM68 somatic clones often from outgrowths in adult wings. The patterning of these outgrowths is similar to an continuous with the part of the wing from which they arise - unlike outgrowths due to clonal expression of dpp, mirror image duplication of pattern in these outgrowth is never seen. The clones producing outgrowths are restricted to the lateral regions of the wing disc whereas those in the central region are of normal size. Lateral clones are morphologically distinct in the late third instar wing disc, and show increased BrdU incorporation levels. There is an increase in apoptosis at the boundaries of brkM68 somatic clones in the wing pouch of third instar wing discs.
Mutant embryos show mislocalisation of crystal cells to more posterior positions in the embryo than normal.
Females containing homozygous germline clones produce wild-type egg chambers and germline stem cells are stable for at least two weeks after clone induction.
Homozygous embryos have normal numbers of abdominal peripheral nervous system neurons in the dorsal and lateral clusters, but fewer in the ventral clusters.
Mutant larvae have narrowed denticle belts which contain about three disordered rows of tapered denticles, which all point to the posterior. The belts usually consist of one row of large denticles followed by two rows of tiny denticles.
In embryos laid by homozygous mutant mothers the leading edge specification is normal.
Embryos show expanded dorsal epidermis at the expense of ventral epidermis. This phenotype resembles that caused by ectopic expression of dpp or of constitutively activated tkv. Mutant clones in the wing disc produce outgrowths and pattern duplications in anterior and posterior regions of the wing. The outgrowths are entirely cell autonomous. Outgrowths are often accompanied by notches, in a similar phenotype to that caused by constitutively activated tkv, though detailed examination of the outgrowths suggests that loss of brk produces a lower level of activation than that caused by constitutively activated tkv.
The ventral denticle belts have largely disappeared due to an expansion of the dorsal epidermis carrying dorsal hairs in brkM68/Y embryos. The number of sna-expressing neuroblasts in the ventral neurogenic region is reduced. The number of amnioserosa cells is normal. The phenotype is not enhanced in embryos derived from females carrying homozygous brkM68 germline clones.
brkM68 has neoplasia | somatic clone | third instar larval stage phenotype, suppressible by Scer\GAL4nub-AC-62/DadUAS.cTa
brkM68 has increased occurrence of cell division | somatic clone | third instar larval stage phenotype, suppressible by Scer\GAL4nub-AC-62/DadUAS.cTa
brkM68 has increased cell number | somatic clone phenotype, non-suppressible by Scer\GAL4nub-AC-62/DadUAS.cTa
brkM68 is a suppressor of abnormal neuroanatomy phenotype of shn1
brkM68 has ventral denticle belt phenotype, enhanceable by tsh8
brkM68 has embryonic abdominal ventral sensory organ precursor cluster group phenotype, non-suppressible by shn1
brkM68 is an enhancer of ventral denticle belt phenotype of tsh8
brkM68 is a suppressor of embryonic abdominal dorsal sensory organ precursor cluster phenotype of shn1
brkM68 is a suppressor of embryonic abdominal lateral sensory organ precursor cluster phenotype of shn1
brkM68, sogY506 has ventral denticle belt phenotype
brkM68, sogY506 has ventral neurectoderm phenotype
The mesoderm is able to spread out over the ectoderm after mesoderm invagination in sogY506 brkM68 double mutant embryos. The mesoderm is able to spread out over the ectoderm after mesoderm invagination in Egfrtop-18A sogY506 brkM68 triple mutant embryos.
Overgrowth of brkM68 somatic clones in lateral regions of wing discs is not suppressed in DadScer\UAS.cTa; Scer\GAL4nub-AC-62 animals.
shn1 brkM68 double mutant embryos show a clear rescue of the number of neurons in the dorsal and lateral clusters of the peripheral nervous system compared to shn1 single mutants. The reduction in the number of neurons in the ventral clusters in shn1 brkM68 double mutant embryos is indistinguishable from that in brkM68 single mutants.
The ectoderm of brkM68 sogY506/Y double mutant embryos forms only dorsal-type cuticle hairs and completely lacks ventral denticles. The ventral neurogenic region is deleted. The amnioserosa defect seen in sogY506/Y single mutant embryos is not rescued in the double mutant embryos. brkM68; dppH46 sna18 Df(2R)twi quadruple mutant embryos secrete cuticles showing partial transformation of ventral into dorsal epidermis.