Deletion in genomic DNA upstream of the LanA gene, from 2.5kb upstream of the translational start site of LanA (site of insertion of progenitor, P{hsneo}AS249) to between nucleotides 370 and 806 of LanA, thereby deleting at least 370 bp of translated sequence of LanA.
viable (with LanAC01-190)
bouton & neuromuscular junction & embryo
embryonic/larval midgut & endoderm
muscle attachment site & basal lamina
Adult-generated LanA9-32 homozygous mutant intestinal stem cell clones have reduced maintenance 7 days and 14 days after clone induction compared to control clones; remaining clones contain fewer cells by day 14.
Embryos mutant for LanA9-32 do not exhibit any salivary gland invagination or migration defects.
The neuromuscular junction (NMJ) is normal in size in LanA9-32/LanAC01-190 mutant larvae.
Expression of LanAGD6022 under the control of Scer\GAL4C57 in a LanA9-32/+ background results in an increase in NMJ size compared to wild type.
Late hemizygous LanA9-32 embryos show normal midgut morphology, but assembly of the extracellular matrix that normally surrounds it is severely disrupted.
Mutant embryos exhibit three defects in cellular organisation: detachment between the amnioserosa and the yolk cell; weak amnioserosa cell thinning; and apical expansion of the amnioserosa cells. However most embryos complete dorsal closure.
Maternal and zygotic mutant embryos have a range of defects. In the most severe cases, embryos disintegrate before the onset of retraction, in milder cases embryos exhibit fusion or deletion of segments and twisting, but no retraction defects.
Homozygous LanA9-32 mutants exhibit a subtle phenotype, revealing midline guidance errors in approximately 4% of segments.
germ-line clones for LanA9-32 generate round eggs at a low frequency.
In a small proportion (4%) of LanA9-32 mosaic egg chambers in which the posterior follicle cells are mutant, the oocyte nuclei remain posterior after stage 8, in contrast to wild-type.
Attachment of muscles to the epidermis is slightly disturbed in stage 16 homozygous embryos. Connecting hemiadherens junctions (HAJs) and tendon HAJs are normal in stage 17 embryos. The basement membrane is present, but is often fragmented and detaches from the unspecialised surfaces of the epidermis and muscles. The basement membrane remains attached to 88% of focal HAJs. The degree of adhesion of neuronal boutons to the muscle surface is reduced at the neuromuscular junctions.
Embryos exhibit significant gaps in the dorsal trunk of the trachea.
Stage 15 and stage 16 Msp-300sz75 LanA9-32 double mutant embryos exhibit complete disruption of the muscle pattern.
The embryonic heart is 'broken', the pericardial cells are loosely associated with each other before dorsal closure and they dissociate from the cardioblasts after dorsal closure and migrate randomly. The somatic myotubules are narrow and twisted and may fall apart. The ventral oblique muscles never reach their proper attachment sites and exhibit an abnormal shape. The initial phase of columnar midgut endoderm polarisation is defective leading to improper arrangement of the endoderm along the visceral mesoderm.
Embryos, which are morphologically normal (with respect to CNS, PNS, motoneurons, muscles, head, mouthparts and denticle bands) and mobile nevertheless fail to hatch.
LanA9-32 has abnormal neuroanatomy phenotype, enhanceable by sliunspecified
LanA9-32 has abnormal neuroanatomy phenotype, suppressible by scbunspecified
LanA9-32/scbunspecified is an enhancer of abnormal neuroanatomy phenotype of sliunspecified
LanA9-32 is an enhancer of abnormal neuroanatomy phenotype of sliunspecified
LanA9-32/LanA[+] is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Scer\GAL4Mhc.PU, fz2UAS.N
LanA9-32 is a suppressor of abnormal neuroanatomy phenotype of scbunspecified
LanA9-32, mys1/mys[+] has abnormal neuroanatomy | third instar larval stage phenotype
LanA9-32, mew[+]/mewM6 has abnormal neuroanatomy | third instar larval stage phenotype
Itgbn1/betaInt-nu[+], LanA9-32/LanAC01-190 has abnormal neuroanatomy | third instar larval stage phenotype
FakN30/FakKG00304, LanA9-32/LanA[+] has abnormal neuroanatomy | third instar larval stage phenotype
Itgbn1/betaInt-nu[+], LanA9-32 has abnormal neuroanatomy | dominant | third instar larval stage phenotype
LanA9-32, scbunspecified, sli2 has abnormal neuroanatomy phenotype
LanA9-32 has fascicle phenotype, enhanceable by sliunspecified/scbunspecified
LanA9-32 has fascicle phenotype, enhanceable by sliunspecified
LanA9-32/LanA[+] is an enhancer of heart primordium phenotype of sli2
sli2/LanA9-32 is an enhancer of fascicle phenotype of scbunspecified
LanA9-32/scbunspecified is an enhancer of fascicle phenotype of sliunspecified
LanA9-32/LanA[+] is a suppressor of neuromuscular junction | third instar larval stage phenotype of Scer\GAL4Mhc.PU, fz2UAS.N
LanA9-32 is a suppressor of central nervous system phenotype of scbunspecified
LanA9-32, mys1/mys[+] has larval dorsal multidendritic neuron ddaC | third instar larval stage phenotype
LanA9-32, mew[+]/mewM6 has larval dorsal multidendritic neuron ddaC | third instar larval stage phenotype
Itgbn1/betaInt-nu[+], LanA9-32/LanAC01-190 has neuromuscular junction | third instar larval stage phenotype
LanA9-32, scb2/scb[+] has embryonic heart cardioblast phenotype
Itgbn1/betaInt-nu[+], LanA9-32 has NMJ bouton | increased number | third instar larval stage phenotype
FakN30/FakKG00304, LanA9-32/LanA[+] has NMJ bouton | increased number | third instar larval stage phenotype
Itgbn1/betaInt-nu[+], LanA9-32 has neuromuscular junction | third instar larval stage phenotype
LanA9-32, scbunspecified has fascicle phenotype
LanA9-32, scbunspecified, sliunspecified has central nervous system phenotype
mys1/LanA9-32 mutant third instar larvae show a mild but statistically significant increase in the proportion of dorsal midline ddaC dendritic length that is enclosed within the epidermis rather than attached to the ECM The amount of enclosed dendrite seen in each heterozygote is similar to wild type.
mewM6/LanA9-32 mutant third instar larvae show a mild but statistically significant increase in the proportion of dorsal midline ddaC dendrite length that is enclosed within the epidermis rather than attached to the ECM. The amount of enclosed dendrite seen in each heterozygote is similar to wild type.
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 LanA9-32.
Significant overgrowth of the NMJ (increased bouton number per muscle area) is seen in LanA9-32/+ 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.
LanA9-32 mutants, when double heterozygous with sliunspecified, exhibit midline crossover of Fas2-labelled axons in over 30% of segments. Midline guidance errors are not visible in LanA9-32/+; scbunspecified/+ double mutants, in contrast to single mutant heterozygotes. However, defasciculation and interruptions to the Fas2-labelling of the most lateral fascicle are observed. The degree of defasciculation and midline guidance errors in all axon tracts of the triple heterozygote of scbunspecified/sliunspecified;LanA9-32/+, appears to be additive of the individual phenotypes. In addition, a narrowing of the central nervous system and the medial displacement of all axon tracts is also seen in this mutant combination.