Imprecise excision of P{EP}EP2030 has produced a 1431bp deletion which includes part of P{EP} and the first 69 codons of βInt-ν.
Posterior midguts from Itgbn1 heterozygous and homozygous adults have a similar proportion of intestinal stem cells to each other and are morphologically indistinguishable from wild-type.
At 22[o]C, homozygous larvae have enlarged neuromuscular junctions (NMJs) (increased bouton number per muscle area) compared to controls. When reared at 29[o]C, the mutant larvae show no further increase in NMJ size, in contrast to wild-type controls, which show enlarged NMJs at 29[o]C compared to at 22[o]C. The mutant larvae do not show an increase in NMJ size after 8 hours food deprivation, in contrast to controls.
Itgbn1 mutant embryonic hemocytes show a decreased competence to undertake phagocytosis of apoptotic cells, despite of no changes in proportions of hemocytes or apoptotic cells in those embryos, as compared to controls.
Itgbn1/betaInt-nu[+] is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Scer\GAL4Mhc.PU, fz2UAS.N
Itgbn1/betaInt-nu[+], LanA9-32/LanAC01-190 has abnormal neuroanatomy | third instar larval stage phenotype
Itgbn1/betaInt-nu[+], LanA9-32 has abnormal neuroanatomy | dominant | third instar larval stage phenotype
FakN30/FakKG00304, Itgbn1/betaInt-nu[+] has abnormal neuroanatomy | third instar larval stage phenotype
Itgbn1/Itgbn1 is an enhancer of anterior midgut primordium phenotype of mys11
Itgbn1/Itgbn1 is an enhancer of embryonic midgut constriction phenotype of mys11
Itgbn1 is an enhancer of salivary gland common duct primordium | maternal effect phenotype of mys11
Itgbn1/Itgbn1 is a non-enhancer of circular visceral muscle primordium | maternal effect phenotype of mys11
Itgbn1/betaInt-nu[+] is a suppressor of neuromuscular junction | third instar larval stage phenotype of Scer\GAL4Mhc.PU, fz2UAS.N
Itgbn1/betaInt-nu[+], LanA9-32/LanAC01-190 has neuromuscular junction | third instar larval stage phenotype
Itgbn1/betaInt-nu[+], LanA9-32 has neuromuscular junction | third instar larval stage phenotype
Itgbn1/betaInt-nu[+], LanA9-32 has NMJ bouton | increased number | third instar larval stage phenotype
FakN30/FakKG00304, Itgbn1/betaInt-nu[+] has neuromuscular junction | third instar larval stage phenotype
FakN30/FakKG00304, Itgbn1/betaInt-nu[+] has NMJ bouton | increased number | third instar larval stage phenotype
βInt-ν1/+ ; LanA9-32/LanAC01-190 third instar larvae show overgrowth of the neuromuscular junction.
The reduction in neuromuscular junction size seen in third instar larvae expressing fz2Scer\UAS.N under the control of Scer\GAL4Mhc.PU is suppressed if they are also heterozygous for βInt-ν1.
Significant overgrowth of the neuromuscular junction (NMJ) (increased bouton number per muscle area and increased NMJ length per muscle area) is seen in βInt-ν1/+ FakN30/FakKG00304 third instar larvae.
Significant overgrowth of the NMJ (increased bouton number per muscle area and increased NMJ length per muscle area) is seen in βInt-ν1/+ LanA9-32/+ third instar larvae.
Midgut constrictions fail to form in mys11; βInt-ν1 double homozygotes. This may be a secondary effect of defects in the visceral muscle surrounding the midgut: the midgut is initially enclosed by visceral muscle, but by stage 16 this muscle becomes highly disorganized and patchy and detaches from the underlying endoderm. (Note these phenotypes are for embryos maternally and zygotically βInt-ν1/βInt-ν1 - zygotic alone not tested). In embryos maternally and zygotically homozygous for mys11 and βInt-ν1, migration of the midgut primordia fails to occur, but disorganization of the visceral mesoderm (circular visceral muscle primordium?) seen in mys11 maternal/zygotic homozygotes in not enhanced. Other mutant phenotypes of mys11 mutant embryos (defects in dorsal closure, germ-band retraction and muscle detachement) are unaffected by βInt-ν1.