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General Information
Symbol
Dmel\RhoGEF21.1
Species
D. melanogaster
Name
FlyBase ID
FBal0085934
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
DRhoGEF21.1
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

C17037153T

Amino acid change:

Q872term | RhoGEF2-PD; Q518term | RhoGEF2-PE; Q872term | RhoGEF2-PF; Q872term | RhoGEF2-PG; Q769term | RhoGEF2-PH

Reported amino acid change:

Q872term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: Q872term.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

RhoGEF21.1 embryos display defects in cellularisation including an irregular, wavy cellularisation front. Despite this RhoGEF21.1 embryos that reach the end of cellularisation look normal. The irregularity of the cellularisation front recovers, particularly in the ventral cells, and both the increased cell depth and basal loss of myosin occur normally in these cells.

In mid-cellularisation embryos derived from RhoGEF21.1 germline clones, the furrow canals are considerably enlarged compared to wild-type and are filled with large cytoplasmic blebs. Interruptions in the regular F-actin array (a hexagonal array is normally evident in surface views) are seen in these embryos and a variable proportion of the forming cells contain multiple nuclei. Embryos derived from RhoGEF21.1 germline clones show normal membrane invagination and nuclear extension during cellularisation.

RhoGEF21.1/RhoGEF24.1 animals show 97% embryonic viability, 96% first larval instar viability and 0% adult viability. Large homozygous clones in the wing disc result in defects in folding of the disc; bifurcations of the folds are found at the boundary between mutant and wild-type tissue.

Homozygous clones contain on average the same number of cells as wild-type twin clones. The planar polarity of bristles in homozygous clones in the wing is normal.

The mitotic pattern in early embryos derived from females containing RhoGEF21.1 germline clones shows the same delay in the ventral domain as in wild-type embryos.

Embryos derived from homozygous female germline clones have normal dorso-ventral and anterior-posterior patterning, and normal mesoderm specification. Germband extension and posterior midgut invagination appear defective. The cells of the mesectoderm fail to intercalate at the ventral midline. Gastrulation is highly disorganised and ventral furrow formation never occurs. Inappropriate lateral folds are formed. Invagination of the anterior midgut is also defective.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Suppressor of
Statement
Reference

RhoGEF21.1 is a suppressor of eye phenotype of Rho1GMR.PH

Other
Additional Comments
Genetic Interactions
Statement
Reference

RhoGEF21.1 shows a weak interaction (5-24% of double heterozygotes have at least one malformed leg) with the following mutations: Sb63b, Sb70. br1 fails to show a significant genetic interaction (assayed in terms of a malformed leg phenotype) with RhoGEF21.1. Sbsbd-201/Sbsbd-1 shows a weak interaction (5-24% of double mutants have at least one malformed leg) with the following mutations: RhoGEF21.1/+.

33% of RhoGEF21.1/zipEbr double heterozygotes have a malformed leg phenotype.

Dominantly suppresses the Rho1GMR.PH rough eye phenotype. The transient depression in the dorsal head region seen in embryos carrying foghkb.PB in a wild-type background is not seen in embryos carrying foghkb.PB which are derived from homozygous RhoGEF21.1 female germline clones.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

Isolated as a dominant suppressor of the Rho1GMR.PH rough eye phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (10)