FB2025_01 , released February 20, 2025
Allele: Dmel\LanA9-32
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General Information
Symbol
Dmel\LanA9-32
Species
D. melanogaster
Name
FlyBase ID
FBal0029903
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
lamA9.32, lamA9-32
Key Links
Nature of the Allele
Cytology
Description

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.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

bouton & neuromuscular junction & embryo

embryonic/larval midgut & endoderm

muscle attachment site & basal lamina

Detailed Description
Statement
Reference

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.

The neuromuscular junction is normal in LanA9-32/LanA216 third instar larvae.

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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
Enhancer of
Statement
Reference

LanA9-32/LanA[+] is an enhancer of visible | dominant phenotype of sogEP11

LanA9-32/LanA[+] is an enhancer of visible | dominant phenotype of sogEP7

Suppressor of
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference

LanA9-32/LanA[+] is an enhancer of heart primordium phenotype of sli2

LanA9-32/LanA[+] is an enhancer of wing vein phenotype of sogEP11

LanA9-32/LanA[+] is an enhancer of wing vein phenotype of sogEP7

NOT Enhancer of
Statement
Reference

LanA9-32/LanA[+] is a non-enhancer of wing phenotype of mys8

Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

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.

LanA9-32/+ ; scb2/+ double heterozygous embryos show defects in alignment of the cardioblasts at the dorsal midline.

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/+; sli2/+ embryos show heart defects that include contralaterally placed cardial cell nuclei and laterally placed cardial cells.

The addition of LanA9-32/+ to mys8 hemizygotes does not enhance the wing blister phenotype seen in these animals.

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.

ifB4 LanA9-32 double mutant embryos show each of the defects seen in ifB4 or LanA9-32 single mutant embryos, and in addition show loss of basement membrane adhesion to the epidermal HAJs.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (26)