Allele Dmel\Rho1^rev220

General Information
Symbol	Dmel\Rho1^rev220	Species	D. melanogaster
Name		FlyBase ID	FBal0102859
Feature type	allele	Associated gene	Dmel\Rho1
Also Known As	Rho^rev220

Allele class
Mutagen
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class
Mutagen
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype	Rho1^k07236 (Magie et al., 1999)
Nature of the lesion	Statement Reference Portion of the Rho1 coding region is removed. (Magie et al., 1999)
Cytology
Phenotypic Data
Phenotypic Class
	cell shape defective (Fox et al., 2005) lethal \| embryonic stage \| maternal effect \| recessive (Magie et al., 1999) lethal \| embryonic stage \| recessive (Magie et al., 1999)
Phenotype Manifest In
	denticle belt \| maternal effect (Magie et al., 1999) dorsal closure embryo (Fox et al., 2005) embryonic/first instar larval cuticle & embryonic head (Fox et al., 2005) embryonic epidermis \| dorsal \| maternal effect (Magie et al., 1999) embryonic epidermis \| maternal effect (Magie et al., 1999) embryonic head (Fox et al., 2005) embryonic head \| maternal effect (Magie et al., 1999) nurse cell ring canal \| maternal effect (Magie et al., 1999) oocyte \| maternal effect (Magie et al., 1999) RP3 motor neuron (Hu et al., 2001)
Detailed Description
	Statement Reference Most Rho1^rev220 mutant embryos lack head cuticle; with the remaining cuticle differing in size among different embryos. Approximately 17.5% of embryos have severe head defects. In 51.5% of the embryos the head is missing, with the entire embryo occupying less than 0.6 of the field at x20 magnification. Rho1^rev220 mutants are nearly normal during early dorsal closure, with defects becoming apparent during late dorsal closure. This phenotype is variable, in more severely affected mutants, both the leading-edge actin cable and cell shape changes are less uniform. In less severely affected mutants, when the leading edges meet at the dorsal midline the two epithelial sheets do not line up or intercalate normally. Approximayely 97.6% of Rho1^rev220 mutants exhibit some kind of head defect or head hole. Less than 1% of Rho1^rev220 mutants are phenotypically wild-type. (Fox et al., 2005) In heterozygous mutants, an occasional loss of the RP3 neuron is seen. (Hu et al., 2001) Mutant embryos die with anterior dorsal hole, and bowed body shape. Head involution fails. The procephalon remains on the exterior giving rise to the anterior dorsal hole in the cuticle. Dorsal midline is puckered, though dorsal closure does occur. Cells on the dorsal midline are inappropriately shaped, pinched or stretched. Homozygous mutant embryos derived from mothers with reduced maternal Rho1 function show both the maternal segmentation phenotype and the zygotic morphogenetic phenotype. (Magie et al., 1999)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference Rho1^rev220 has lethal \| dominant \| embryonic stage \| maternal effect phenotype, enhanceable by capu¹ (Magie et al., 1999) Rho1^rev220 has lethal \| dominant \| embryonic stage \| maternal effect phenotype, enhanceable by capu² (Magie et al., 1999)
Suppressed by
Statement Reference Rho1^rev220 has cell shape defective phenotype, suppressible \| partially by Scer\GAL4^Act5C.PU/p120ctn^Scer\UAS.cFa (Fox et al., 2005)
NOT Suppressor of
Statement Reference Rho1^rev220/Rho1[+] is a non-suppressor of neuroanatomy defective \| heat sensitive phenotype of N^l1N-ts1 (Song and Giniger, 2011)
Phenotype Manifest In
Enhanced by
Statement Reference Rho1^rev220 has embryonic/first instar larval cuticle phenotype, enhanceable by p120ctn³⁰⁸ (Fox et al., 2005) Rho1^rev220 has phenotype, enhanceable by cta⁴ (Magie et al., 1999) Rho1^rev220 has phenotype, enhanceable by cta⁵ (Magie et al., 1999)
NOT Enhanced by
Statement Reference Rho1^rev220 has embryonic/first instar larval cuticle & embryonic head phenotype, non-enhanceable by p120ctn³⁰⁸ (Fox et al., 2005) Rho1^rev220 has phenotype, non-enhanceable by aop¹ (Magie et al., 1999) Rho1^rev220 has phenotype, non-enhanceable by arm³ (Magie et al., 1999) Rho1^rev220 has phenotype, non-enhanceable by bsk¹ (Magie et al., 1999) Rho1^rev220 has phenotype, non-enhanceable by chic⁰¹³²⁰ (Magie et al., 1999) Rho1^rev220 has phenotype, non-enhanceable by Egfr^E1 (Magie et al., 1999) Rho1^rev220 has phenotype, non-enhanceable by Egfr^f2 (Magie et al., 1999) Rho1^rev220 has phenotype, non-enhanceable by hep^r75 (Magie et al., 1999) Rho1^rev220 has phenotype, non-enhanceable by puc^E69 (Magie et al., 1999) Rho1^rev220 has phenotype, non-enhanceable by RhoGEF2^unspecified (Magie et al., 1999) Rho1^rev220 has phenotype, non-enhanceable by wg^NZ (Magie et al., 1999)
Suppressed by
Statement Reference Rho1^rev220 has dorsal closure embryo phenotype, suppressible \| partially by Scer\GAL4^Act5C.PU/p120ctn^Scer\UAS.cFa (Fox et al., 2005) Rho1^rev220 has embryonic/first instar larval cuticle & embryonic head phenotype, suppressible \| partially by Scer\GAL4^Act5C.PU/p120ctn^Scer\UAS.cFa (Fox et al., 2005) Rho1^rev220 has embryonic head phenotype, suppressible \| partially by Scer\GAL4^Act5C.PU/p120ctn^Scer\UAS.cFa (Fox et al., 2005)
NOT suppressed by
Statement Reference Rho1^rev220 has embryonic/first instar larval cuticle & embryonic head phenotype, non-suppressible by p120ctn³⁰⁸ (Fox et al., 2005) Rho1^rev220 has phenotype, non-suppressible by aop¹ (Magie et al., 1999) Rho1^rev220 has phenotype, non-suppressible by arm³ (Magie et al., 1999) Rho1^rev220 has phenotype, non-suppressible by bsk¹ (Magie et al., 1999) Rho1^rev220 has phenotype, non-suppressible by chic⁰¹³²⁰ (Magie et al., 1999) Rho1^rev220 has phenotype, non-suppressible by Egfr^E1 (Magie et al., 1999) Rho1^rev220 has phenotype, non-suppressible by Egfr^f2 (Magie et al., 1999) Rho1^rev220 has phenotype, non-suppressible by hep^r75 (Magie et al., 1999) Rho1^rev220 has phenotype, non-suppressible by puc^E69 (Magie et al., 1999) Rho1^rev220 has phenotype, non-suppressible by RhoGEF2^unspecified (Magie et al., 1999) Rho1^rev220 has phenotype, non-suppressible by wg^NZ (Magie et al., 1999)
Enhancer of
Statement Reference Rho1^rev220 is an enhancer of embryonic/first instar larval cuticle phenotype of shg^g119 (Fox et al., 2005) Rho1^rev220 is an enhancer of embryonic ventral epidermis phenotype of shg^g119 (Fox et al., 2005)
Suppressor of
Statement Reference Rho1^rev220 is a suppressor \| partially of embryonic/first instar larval cuticle phenotype of shg² (Fox et al., 2005) Rho1^rev220 is a suppressor of embryonic/first instar larval cuticle phenotype of shg^R69 (Fox et al., 2005) Rho1^rev220 is a suppressor of intersegmental nerve phenotype of Scer\GAL4^elav.PLu, plexB^Scer\UAS.cHa (Hu et al., 2001) Rho1^rev220 is a suppressor of RP3 motor neuron phenotype of Scer\GAL4^elav.PLu, plexB^Scer\UAS.cHa (Hu et al., 2001)
NOT Suppressor of
Statement Reference Rho1^rev220/Rho1[+] is a non-suppressor of intersegmental nerve \| heat sensitive phenotype of N^l1N-ts1 (Song and Giniger, 2011) Rho1^rev220/Rho1[+] is a non-suppressor of intersegmental nerve branch ISNb of A1-7 \| heat sensitive phenotype of N^l1N-ts1 (Song and Giniger, 2011) Rho1^rev220/Rho1[+] is a non-suppressor of segmental nerve branch SNa of A1-7 \| heat sensitive phenotype of N^l1N-ts1 (Song and Giniger, 2011)
Other
Statement Reference Rho1^rev220, RpII140^wimp has egg chamber phenotype (Magie et al., 1999) Rho1^rev220, RpII140^wimp has nurse cell ring canal phenotype (Magie et al., 1999) Rho1^rev220/Rho1[+], RpII140^wimp has egg chamber phenotype (Magie et al., 1999) Rho1^rev220/Rho1[+], RpII140^wimp has nurse cell ring canal phenotype (Magie et al., 1999)
Additional Comments
Genetic Interactions
Statement Reference Heterozygosity for Rho1[rev220] fails to suppress the axonal defects found in N[l1N-ts1] mutants. (Song and Giniger, 2011) Most embryos double mutant for p120ctn³⁰⁸ and Rho1^rev220 lack head cuticle, with the remaining cuticle differing significantly in size among different embryos. p120ctn³⁰⁸ does not substantially modify the Rho1^rev220 phenotype, nor is a novel double-mutant phenotype observed. The percentage of embryos with head holes is similar, for example 76.1% of Rho1^rev220 mutants versus 74.6% of double mutants. However double mutants do have twice as many long cuticles as Rho1^rev220 single mutants. Rho1^rev220 p120ctn³⁰⁸ double mutants exhibit the same range of phenotypes as Rho1^rev220 single mutants during early and later stages of dorsal closure. Overexpression of p120ctn^Scer\UAS.cFa under the control of Scer\GAL4^Act5C in a Rho1^rev220 background may result in slight suppression of the Rho1^rev220 phenotype (although this may be due to differences in the genetic background). Loss of Rho1^rev220 enhances the shg^g119 phenotype. Most double mutants have holes in their ventral epidermis that are not present in most shg^g119 single mutants. As both Rho1^rev220 and shg^g119 affect head involution, the enhancement of this phenotype may simply reflect additive effects. However, because loss of Rho1^rev220 does not affect integrity of the ventral epidermis, enhancement of this aspect of the phenotype is likely to reflect a genetic interaction. Rho1^rev220 enhances the weak shg^g119 phenotype, leading to more severe embryonic defects. The percentage of phenotypically-wild-type embryos is reduced from approximately 7.6% in shg^g119 embryos to approximately 0.5% in shg^g119 Rho1^rev220 mutants. The majority of shg^g119 Rho1^rev220 mutants (approximately 54%) exhibit ventral holes in the embryonic cuticle, compared to 21.7% in shg^g119 mutants and 0.4% in Rho1^rev220 mutants. The shg² embryonic cuticle phenotype is partially suppressed by Rho1^rev220. Approximately 4.5% of shg² mutants are phenotypically wild-type, while 5.9% of Rho1^rev220 shg² double mutants are wild-type. Approximately 39.9% of double mutants exhibit ventral holes in the cuticle compared to 11.4% in the single shg²¹ mutant, with 55% of shg² mutants exhibiting fragmentary ventral cuticle, while only 46.3% of the double mutants exhibit this phenotype. In summary, over 80% of Rho1^rev220 shg² double mutants have ventral holes or fragmentary ventral cuticle. This illustrates the general suppression of the shg² phenotype in a Rho1^rev220 background. (Fox et al., 2005) Females with reduced Rho1 function (Rho1^rev220/+; +/RpII140^wimp) show disrupted actin cytoskeletal structure in the egg chambers, particularly in the outer ring canals and oocyte cortex. The inner ring canals appear relatively normal. Embryos derived from mothers with reduced Rho1 function die with moderate segmentation defects as seen by denticle belt fusions. Approximately 10% of the dead embryos have cuticular holes that are randomly placed, as opposed to being dorsal. Cell morphology is abnormal with cells showing irregular shapes. Gastrulation is not blocked. (Magie et al., 1999)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	Rho1²²⁰ (Wang and Riechmann, 2007) Rho1^rev220 (Fox et al., 2005, Song and Giniger, 2011) Rho^rev220 (Hu et al., 2001, Magie et al., 1999)
Name Synonym
Secondary FlyBase IDs

References ( 6 )
Research paper	Song and Giniger, 2011, Dev. Dyn. 240(2): 324--332 Noncanonical notch function in motor axon guidance is mediated by Rac GTPase and the GEF1 domain of trio. [FBrf0212819] Wang and Riechmann, 2007, Curr. Biol. 17(15): 1349--1355 The role of the actornyosin cytoskeleton in coordination of tissue growth during Drosophila oogenesis. [FBrf0200870] Fox et al., 2005, Development 132(21): 4819--4831 Rho1 regulates Drosophila adherens junctions independently of p120ctn. [FBrf0190288] Magie et al., 2002, Development 129(16): 3771--3782 Rho1 interacts with p120(ctn) and alpha-catenin, and regulates cadherin-based adherens junction components in Drosophila. [FBrf0151270] Hu et al., 2001, Neuron 32(1): 39--51 Plexin b mediates axon guidance in Drosophila by simultaneously inhibiting active rac and enhancing rhoa signaling. [FBrf0139777] Magie et al., 1999, Development 126(23): 5353--5364 Mutations in the Rho1 small GTPase disrupt morphogenesis and segmentation during early Drosophila development. [FBrf0111959]

Allele Dmel\Rho1rev220

Allele Dmel\Rho1^rev220