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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes

Mutation is a deletion. Upstream breakpoint is in the first intron after amino acid 52. The distal breakpoint is unknown but extends past the coding region.

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

The Rho1 coding region C -terminal to amino acid 52 has been removed.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Hemocytes trans-migrate properly from the head to tail in Rho11B mutant embryos. However, fewer of the tail hemocytes migrate anteriorly along the midline in mutants than in wild-type.

Hemocytes in Rho11B mutant embryos expressing Rho1KDQ.AAA exhibit normal head-to-tail trans-migration. However, the mutant embryos exhibit defects in hemocyte-migration from the tail. There is a significant reduction in the number of hemocytes that migrate anteriorly from the tail along the ventral midline compared with wild-type.

Hemocytes in Rho11B mutant embryos expressing Rho1F39V exhibit normal developmental migration.

The majority of salivary glands partially invaginate in homozygous embryos, but fail to turn and migrate posteriorly. Homozygous salivary gland cells observed at the stage when in wild type all gland cells have invaginated but migration has not yet started do not contract in the apical-basal axis and do not migrate dorsally, in contrast to the behaviour seen in wild-type cells at this stage.

The circular visceral mesoderm is discontinuous in homozygous embryos at a stage where it is continuous in wild-type embryos, with clusters of cells at discrete intervals along the anterior-posterior axis.

Most mutant embryos have a dilated or irregular Filzkorper, especially at the most distal part of the tube (penetrance is 75.8% in zygotic Rho11B mutants and is 69% in embryos that are both maternally and zygotically mutant for Rho11B). Approximately 4% of zygotic Rho11B mutants and 13% of embryos that are both maternally and zygotically mutant for Rho11B show a complete failure in spiracle cell invagination, with the Filzkorper forming on the surface of the embryo.

Stage 17 Rho11B/Rho172R embryos show partial disruption of the cortical actin cytoskeleton in the spiracular chamber.

Maternal mutants exhibit general endocytosis defects.

In contrast to wild type embryos, Rho11B mutant embryos fail to recruit hemocytes to a laser-induced wound after one hour: most Rho11B hemocytes in the locality of the wound are polarized toward it, but are abnormally elongated and are held back by cytoplasmic tethers. Occasionally, very elongated Rho11B cells appear to 'snap free' of their tails and leave a trail of membrane/cytoplasm behind them.

Hemocytes in Rho11B mutant embryos exhibit persistent links to one another whereas cell-cell contacts in wild type embryos are transient.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Phenotype Manifest In
Additional Comments
Genetic Interactions

Rho11B hemizygosity partially suppresses the embryonic lethality and dorsal closure defects seen in embryos expressing crbY10A in a crbGX24w-/crbGX24w- background.

After single cell wounding (by laser ablation), Rho11B, RpII140wimp embryos show defects in assembling an organized actin ring, display a narrowed actin halo area, and wounds expand excessively due to delayed actin recruitment. Actin cortical flow toward the wound is not disrupted.

Oocytes of washΔ185 Rho11B transheterozygous females undergo premature cytoplasmic streaming. The normal gradient of microtubule organisation that is seen in wild-type oocytes at stage 7 is lost in the mutant oocytes. The mutant stage 7 oocytes have disruptions in the cortical actin.

Stage 8 oocytes from capu1/+; Rho11B/+ and Rho11B; RpII140wimp mothers exhibit premature ooplasmic streaming and subcortical arrays of microtubules. In oocytes of both genotype, stable microtubules are restricted to the cortex, as in wild-type oocytes, but differ in the lack of reduction of microtubules at the posterior pole.

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by

Rho1cVa fully rescues the maternal and zygotic phenotypes in hemocytes of Rho11B.

Expression of Rho1Scer\UAS.cHa under the control of one of Scer\GAL4fkh.PH, Scer\GAL4en-e16E or Scer\GAL4wg.PM partially rescues the salivary gland migration defects of Rho11B embryos, with the greatest rescue being seen when expression is driven by Scer\GAL4en-e16E.

Expression of Rho1Scer\UAS.cHa under the control of one of either Scer\GAL4twi.PB or Scer\GAL4bap.PB partially rescues the salivary gland migration defects of Rho11B embryos.

Expression of Rho1Scer\UAS.cMa specifically in the hemocytes (using the Scer\GAL4crq.PA driver) resuces the hemocyte recruitment defect seen in Rho11B mutants.

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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (15)