FB2024_03 , released June 25, 2024
Allele: Dmel\hoip1
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General Information
Symbol
Dmel\hoip1
Species
D. melanogaster
Name
FlyBase ID
FBal0291685
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Amino acid replacement: G37E.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

G9700106A

Reported nucleotide change:

G?A

Amino acid change:

G37E | hoip-PA; G37E | hoip-PB

Reported amino acid change:

G37E

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
Detailed Description
Statement
Reference

hoip1 mutant embryos display defective myotube elongation of a subset of somatic myotubes, including the lateral longitudinal (LL1), dorsal oblique (DO3-5), lateral transverse (LT1-4) and lateral oblique (LO1); the dorsal oblique muscle 2 is decreased in size, despite elongating normally; these embryos also display defects in myoblast fusion and sarcomere assembly.

Somatic muscle morphology is aberrant in homozygous hoip1 mutant embryos compared to heterozygous controls. In particular, the lateral transverse (LT1-4), lateral longitudinal (LL1), lateral oblique (LO1) and dorsal oblique (DO3-5) remain rounded rather than showing pronounced membrane extensions towards target sites as in wild type. Embryos fail to emerge from the chorion after embryogenesis. No PNS defects are detected.

Somatic muscle morphology is aberrant in hoip1/Df(2L)ED690 mutant embryos compared to wild type. In particular, the lateral transverse (LT1-4), lateral longitudinal (LL1), lateral oblique (LO1) and dorsal oblique (DO3-5) remain rounded rather than showing pronounced membrane extensions towards target sites as in wild type. Embryos fail to emerge from the chorion after embryogenesis.

Somatic muscle morphology is aberrant in hoip1/hoipk07104 mutant embryos compared to wild type. In particular, the lateral transverse (LT1-4), lateral longitudinal (LL1), lateral oblique (LO1) and dorsal oblique (DO3-5) remain rounded rather than showing pronounced membrane extensions towards target sites as in wild type. Embryos fail to emerge from the chorion after embryogenesis. No PNS defects are detected.

Unlike in wild type nascent myotubes fail to elongate in hoip1 mutant embryos after 30 minutes, even though the myotubes show an initial polarity. Wild type myotubes elongate to 50% of segment width after 30 minutes but hoip1 mutant embryos even after 60 minutes. By this stage they have lost their polarity. hoip1 mutants do not show any defects in attachment site recognition; as in wild type they extend filopodia exclusively in the direction of myotube polarity. Founder cell specification and the first round of myoblast fusion proceed normally in homozygous hoip1 mutant embryos but the later rounds of fusion do not occur. However, the lack of fusion and elongation defects do not always correlate; DO1 and DA1 muscles elongate normally in hoip1 embryos but have fewer nuclei, whereas LL1 and LO5 are multinucleate but fail to elongate.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
Statement
Reference
NOT suppressed by
Additional Comments
Genetic Interactions
Statement
Reference

Expression of Tm21.Scer\UAS.T:Avic\GFP-EGFP or Tm22.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4kirre-rP298 when expressed at high levels is able to significantly partially rescue the lateral longitudinal and lateral transverse muscle myotube elongation defects of hoip1 mutant embryos, and when expressed at low levels is able to partially rescue the lateral transverse (but not lateral longitudinal) muscle myotube elongation defects of hoip1 mutant embryos.

Expression of Tm23.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4kirre-rP298 when expressed at high levels is able to significantly partially rescue the lateral longitudinal (but not lateral transverse) muscle myotube elongation, dorsal oblique muscle 2 size, sarcomere assembly and myoblast fusion defects of hoip1 mutant embryos, but when expressed at low levels is unable to rescue the lateral longitudinal or lateral transverse muscle myotube elongation or sarcomere assembly defects of hoip1 mutant embryos.

Expression of 2 copies of Tm2cDNA.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4kirre-rP298 is able to significantly rescue the lateral longitudinal and lateral transverse muscle myotube elongation defects of hoip1 mutant embryos.

Expression of Mhc+memb is unable to suppress the somatic muscle morphology defects seen in hoip1 mutant embryos.

Xenogenetic Interactions
Statement
Reference

Expression of Hsap\NHP2L1Scer\UAS.cJa in founder cells under the control of Scer\GAL4kirre-rP298 significantly rescues the myotube elongation defects seen in hoip1 mutant embryos.

Complementation and Rescue Data
Fails to complement
Comments

Expression of hoipScer\UAS.cJa under the control of Scer\GAL4kirre-rP298 rescues the myotube elongation defects seen in hoip1 mutant embryos.

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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (2)