Insertion in an intron of Rho1.
Rho1k02107b homozygotes are lethal, pupae are abnormally thin but third instar larvae present no obvious muscle phenotype, as compared to controls.
The majority of salivary glands fail to invaginate in homozygous embryos, with the cells remaining at the ventral surface of the embryo. These invagination defects are first observed in late stage 11. In those mutant embryos where the salivary glands do invaginate, invagination always starts at the correct dorsal-posterior position.
The salivary gland epithelium of homozygous embryos consists of mesenchymal shaped cells with disorganised cortical F-actin (in contrast to control cells, which are columnar in shape and have prominent cortical F-actin).
Rho1k02107b/Df(2R)Jp1 embryos show defects in salivary gland migration and invagination.
Mutant embryos show a lack of peripheral glial sheaths in the lateral region of the embryo and loss of glia at the CNS/PNS transition zone.
Strong allele.
GluRIIASP16, Rho1[+]/Rho1k02107b has abnormal neurophysiology | third instar larval stage | recessive phenotype, non-enhanceable by ExnEY01953/Exn[+]
Rho1[+]/Rho1k02107b is an enhancer of visible | dominant phenotype of Sb70
Rho1[+]/Rho1k02107b is an enhancer of visible | dominant phenotype of br1
Rho1[+]/Rho1k02107b is an enhancer of visible | dominant phenotype of Sb63b
Rho1[+]/Rho1k02107b is an enhancer of visible phenotype of br1
Rho1[+]/Rho1k02107b is a suppressor of chemical resistant phenotype of RhoGAP18B1
Rho1[+]/Rho1k02107b is a suppressor of visible phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E
GluRIIASP16, Rho1[+]/Rho1k02107b has abnormal neurophysiology | recessive | third instar larval stage phenotype
E(br)121Ebr121, Rho1[+]/Rho1k02107b has visible | dominant phenotype
E(br)444Ebr444, Rho1[+]/Rho1k02107b has visible | dominant phenotype
E(br)121Ebr121/E(br)121[+], Rho1k02107b has visible phenotype
E(br)444[+]/E(br)444Ebr444, Rho1k02107b has visible phenotype
GluRIIASP16, Rho1[+]/Rho1k02107b has embryonic/larval neuromuscular junction phenotype, non-enhanceable by ExnEY01953/Exn[+]
Rho1k02107b has presumptive embryonic salivary gland phenotype, suppressible by Scer\GAL4fkh.PH/crbUAS.cWa
Rho1k02107b has presumptive embryonic salivary gland phenotype, suppressible by Scer\GAL4fkh.PH/RokCAT.UAS
Rho1[+]/Rho1k02107b is an enhancer of leg phenotype of Sb70
Rho1[+]/Rho1k02107b is an enhancer of leg phenotype of br1
Rho1[+]/Rho1k02107b is an enhancer of leg phenotype of Sb63b
Rho1k02107b is a suppressor of ectoderm | extended germ band stage phenotype of upd1YM55
Rho1[+]/Rho1k02107b is a suppressor of wing phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E
GluRIIASP16, Rho1[+]/Rho1k02107b has embryonic/larval neuromuscular junction phenotype
E(br)121Ebr121, Rho1[+]/Rho1k02107b has leg phenotype
E(br)444Ebr444, Rho1[+]/Rho1k02107b has leg phenotype
E(br)121Ebr121, Rho1k02107b has leg phenotype
E(br)444Ebr444, Rho1k02107b has leg phenotype
An average of 6% osupd-4, Rho1k02107b homozygous mutant embryos show germ-band extension defects, much reduced compared to osupd-4 homozygous mutant embryos.
The Rho1k02107b/+ heterozygous mutation can partially suppress the GluRIIASP16 NMJ synaptic homeostatic response.
The ExnEY01953/+ heterozygous mutation does not enhance the Rho1k02107b/+, GluRIIASP16 double mutant NMJ synaptic homeostasis phenotype.
Expression of crbScer\UAS.cWa under the control of Scer\GAL4fkh.PH partially suppresses the salivary gland invagination defects of Rho1k02107b embryos; the fraction of non-invaginated glands decreases from 80% to 68%, and the fraction of partially invaginated glands increases from 18% to 29%.
Expression of rokCAT.Scer\UAS under the control of Scer\GAL4fkh.PH partially suppresses the salivary gland invagination defects of Rho1k02107b embryos.
Heterozygosity for Rho1k02107b or Df(2R)Jp6 (which removes Rho1) strongly suppresses the RhoGAP18B1 ethanol-resistance phenotype.
Rho1k02107b/+ suppresses the mutant wing phenotype caused by expression of LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E (the % of wings with normal morphology at 18oC is increased from 9% to 95%). The frequency of the malformed leg phenotype seen in Sb63b/+ heterozygotes (8%) is increased if the flies are also heterozygous for Rho1k02107b (93%). The frequency of the malformed leg phenotype seen in Sb70/+ heterozygotes (7%) is increased if the flies are also heterozygous for Rho1k02107b (95%). The frequency of the malformed leg phenotype seen in br1/Y males (1%) is increased if the flies are also heterozygous for Rho1k02107b (55%).
Dominantly enhances the frequency of br1 mutant animals with malformed legs. The fraction of flies showing a malformed leg phenotype in at least one leg, for Rho1k02107b in double heterozygous combination with one of the following alleles is - SbEbr20 : 8%, SbEbr48 : 2%, SbEbr228 : 12%, SbEbr448 : 2%, SbEbr536 : 10%, SbEbr623 : 2%, bsEbr292 : 0%, E(br)24Ebr24 : 3%, E(br)65Ebr65 : 6%, E(br)155Ebr155 : 0%, E(br)165Ebr165 : 7%, E(br)333Ebr333 : 6%, E(br)72Ebr72 : 5%, E(br)121Ebr121 : 56%, E(br)160Ebr160 : 8%, E(br)187Ebr187 : 2%, E(br)420Ebr420 : 2% and E(br)444Ebr444 : 37%.
Rho1k02107b is partially rescued by Scer\GAL4fkh.PH/Rho1UAS.cHa
Expression of Rho1Scer\UAS.cHa under the control of Scer\GAL4fkh.PH partially rescues the salivary gland defects of Rho1k02107b embryos; with the fraction of non-invaginated glands decreasing from 80% to 27% and the fraction of completely invaginated glands increasing from 2% to 58%.
I. Kiss.
This allele was listed in the BDGP database as a lethal or sterile line during the period 1994-1999, but was discarded from the gene disruption project prior to the summary publication (FBrf0111489). Reasons for excluding lines from the collection described in FBrf0111489 include presence of more than one P insertion on the mutant chromosome, separation of lethality (or sterility) from the location of the insertion, and loss of lethality (or sterility) from the stock. Further information is available from http://www.fruitfly.org/bfd/ and from Dr. Spradling (spradling@mail1.ciwemb.edu).
Complements: l(2)0507005070. Complements: l(2)44DEa05847. Complements: ptck02507. Complements: l(2)44DEak05512. Complements: spink06110. Complements: Vps25k08904. Complements: spink09905. Complements: l(2)k15617k15617. Complements: l(2)s1878s1878.