|Feature type||allele||Associated gene||Dmel\phl|
|Also Known As||D-Raf11-29, raf11-29, Draf11-29, raf1129, l(1)phl11-29, l(1)ph11-29|
|Map ( GBrowse )|
|Allele class||loss of function allele, amorphic allele - genetic evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Intragenic insertion, between amino acids 252 and 466, of 3.6kb, causing truncation of phl protein.
4kb DNA insertion.
|Phenotype Manifest In|
Embryos derived from females containing homozygous germline clones have an abnormal cuticle pattern with deletion of posterior structures (abdominal segment 8 and Filzkorper).
Hemizygous larvae have fewer hemocytes than wild-type larvae.
Embryos derived from phl11 female germ line clones exhibit defective gastrulation and lack the posterior midgut primordium. The majority of pole cells in these mutants are unable to enter the embryo at gastrulation and those that do enter the embryo appear abnormal in both directed migration and aggregation, leading to their random scattering in the embryonic cavity.
In phl11 mutant somatic clones in the 3rd instar eye disc, photoreceptors R2-R5 fail to undergo or differentiation. Within phl11 mutant somatic clones there is a failure of G1 arrest in the furrow: all cells except R8s re-enter the cell cycle. However, none of these cells progress past G2.
The percentage of lamellocytes in the circulating blood cells of third instar larvae is strongly reduced in phl11 mutants compared to wild type. In addition, the total concentration of circulating blood cells is greatly reduced in the mutant larvae compared to wild type.
Border cells show normal migration during stage 9 when all dorsal follicle cells are mutant for phl11 in females containing homozygous clones. Mutant clusters are rarely recovered at stage 10, but dorsal migration can occur, although in most cases the cells probably die or cause the egg chamber to degenerate at stage 10.
phl11/Y embryos show loss of VA2 muscle precursor cells (only 1.2% of hemisegments contain VA2 precursor cells). The embryos have a twisted morphology.
Paternally rescued embryos derived from females with homozygous germline clones (lacking maternal but not zygotic Egfr function) lack head and tail structures at 24 hours. The embryos appear twisted at 6 hours of development. Hemizygous embryos derived from females with homozygous germline clones (lacking both maternal and zygotic Egfr function) produce what appears to be a small patch of dorsal cuticle at the end of embryonic development. The embryos appear twisted at 10 hours of development.
Multiple R8 cells are specified in an abnormal pattern in homozygous clones.
phl11 males which have been partially rescued by expression of phlwt.hs (phlwt.hs has not been provided during the second and third larval instars) show a mirror-image duplication of the anterior compartment in the posterior of the wing disc. These animals show duplication of anterior pattern elements in the posterior compartment of the wing when allowed to reach adulthood. Comparable pattern duplications are also seen in the legs.
phl11 mutants are lethal in larvae, but such flies carrying phlhs.PD can survive to fertile adults by using daily heatshocks. If heatshocks are withdrawn on eclosion, testes from 5 day old males are indistinguishable from controls. By day 7 however, almost all mutant testes show great proliferation centre expansion. This is due to excess, early stage germ cells and continues such that on day 15 testes are filled with these cells at the expense of post-mitotic cells. In these mutants fusome structure is not normal. Unbranched fusomes are found in may cells even those located some distance from the hub, where in wild-type testes, only branched fusomes interconnecting secondary spermatogonia are found. Although branches fusomes are found, these fusomes usually appear only after an intervening region containing many excess cells that have only spheroid fusomes. These excess germ-cells do not result from an increased frequency of germline stem cell divisions, as the M-phase index for the tier of cells adjacent to the hub in mutant testes is almost identical to that in wild-type. However the germ-line stem cells as a population appear to remain active longer than seen in wild-type.
Hemizygotes and homozygotes die as third instar larvae lacking imaginal discs.
Homozygous embryos exhibit defects in posterior pattern.
Homozygous embryos lack head and tail structures.
Null embryos from homozygous female germlines differentiate remnants of cuticle with no obvious pattern. Embryos from homozygous germlines that receive a paternal wild type phl have cuticles that resemble those of embryos from tor mutant females.
Class 1 allele: Unrescued embryos (lacking maternal and zygotic phl activity) fail to differentiate into structured embryos and degenerate around 7 hrs of development. Rescued embryos (carrying wild type phl from their father) miss most structures posterior to abdominal segment 6 or 7 and anteriorly a portion of the cephalopharyngeal skeleton, labral sense organ and medial tooth are deleted. fkh expression (in wild type evident in hindgut, Malpighian tubule(s) and anal pads) entirely absent from class 1 embryos. Expression of tll, hkb, hb, fkh absent from both rescued and unrescued embryos, 7th ftz stripe deleted and 6th ftz stripe variably deleted/expanded. Conclude from 0% to 20--25% EL of blastoderm embryos deleted in class 1 alleles.
A hole is seen in the blastoderm layer below the pole cells in embryos. Ventral furrow formation extends posteriorly to approximately 5% egg length. The posterior midgut invagination does not occur. 10% of embryos twist along the dorsal-ventral axis at germband extension to produce corkscrew shaped embryos. Comparison of embryos derived from homozygous germline clones reveal a zygotic requirement for phl: "pole hole" embryos (which have zygotic phl function) undergo germ band shortening and show the "terminal class" phenotype upon completing development. Posterior phenotype: A deletion of terminal identities is observed and cells forming in this region assume more anterior fates. The remaining most posterior segments (typically A5, A6 and A7) are expanded. This altered segmental pattern is first seen at the blastoderm stage. Deformation of the CNS ladder is observed for many embryos after nerve cord condensation. Usually the anterior and posterior commissures are normal in the last complete terminal segment, but breaks in the longitudinal axis of the CNS are seen. In some cases the sensory cells of the PNS are displaced laterally in the expanded abdominal segments. In addition, fusion of the dorsal cell cluster along the dorsal midline is observed, and the positions of the lateral chordotonal organs are shifted dorsally in the most posterior complete segment of the embryo. Anterior phenotype: Several head defects are also apparent in mature "pole hole" embryos, these arise in structures derived from the labrum and acron. Much of the supraoesophageal ganglia (brain) is missing at 16 hours. The optic lobes are also altered. The labral sense organ (epiphysis) is missing. Cell death is seen in the head and tail regions. In contrast, although "null" embryos (which have no zygotic phl function) appear phenotypically equivalent to "pole hole" embryos until the completion of germband extension, development ceases at this elongated germband stage, and they do not undergo germband shortening. After 20 hours of development the embryos consist of a ball of embryonic tissue at the anterior egg pole, and an extruded mass of egg yolk at the posterior pole. The overall organisation and differentiation of organ systems within the embryo is abnormal, due to incomplete development and massive cell death. The development of the nervous system is severely affected.
|NOT Enhancer of|
|NOT Suppressor of|
|Phenotype Manifest In|
phl11 has A1-7 ventral acute muscle 2 | precursor phenotype, suppressible | partially by Scer\GAL4twi.PG/csw::Src64Bsrc90.Scer\UAS
|NOT suppressed by|
|NOT Enhancer of|
phl11/phl[+] is a suppressor of eye photoreceptor cell | ectopic phenotype of PDZ-GEFEP388, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
phl11/phl[+] is a suppressor of ommatidium phenotype of PDZ-GEFEP388, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
phl11 is a suppressor | maternal effect of embryonic/first instar larval cuticle | maternal effect phenotype of tor12D
|NOT Suppressor of|
phl11 sl1 double mutant border cell clusters (induced as clones) initiate migration, but are delayed later in posterior migration and do not show dorsal migration. phl11 sl1 double mutant cells are generally located at the rear of the cluster during border cell late posterior migration and dorsal migration in mosaic border cell clusters consisting of both wild-type and mutant cells.
Caspase activation is seen posterior to column 5, Within phl11 mutant clones in the eye disc in a BacA\p35GMR.PH background, caspase activation is seen posterior to column 5 relative to the morphogenetic furrow. There is no increase in caspase activation outside of these clones.
The rough eye phenotype, irregular ommatidial array and increased photoreceptor cell number caused by expression of Gef26EP388 under the control of Scer\GAL4GMR.PF are strongly suppressed by phl11/+.
At 28oC, the increased differentiation of blood cells into lamellocytes and the increased accumulation of blood cells seen in hopTum larvae is completely suppressed by phl11. All hemizygous phl11 hopTum larvae have overgrown and melanised lymph glands, similar to that seen in hopTum mutants cultured at 28oC.
Expression of csw::Src64Bsrc90.Scer\UAS under the control of Scer\GAL4twi.PG partially suppresses the loss of VA2 muscle precursor cells seen in phl11/Y embryos (10.5% of hemisegments have VA2 cells).
At 25oC phl11 dominantly suppresses most of the hyperplastic growth seen in Ras85DV12.Scer\UAS Scer\GAL4dpp.blk1 wing discs.
|Complementation & Rescue Data|
|Partially rescued by|
|Not rescued by|
phl[ΔN114.Hsp83] can rescue the posterior defects seen in embryos derived from derived from females containing homozygous phl germline clones (rescue is seen if the level of expression from the transgene is equal or greater than the endogenous wild-type level of phl protein), but phl[ΔN114.Hsp83] is less active than phl[Hsp83.PD] in this assay (the latter can rescue the posterior defects at much lower levels of expression).
Expression of phlwt.hs using daily heat shocks from embryonic through late pupal stages rescues phl11 males to full viability and fertility.
Injection of wild type RNA rescues the filzkorper, tuft and anal pads.
Injection of wild type phl transcripts into the posterior region of phl11 embryos rescues the posterior and injection into the head region rescues the anterior terminal structures. Injection of phlK497M into the anterior or posterior pole of phl11 embryos rescues neither the head nor tail defects.
|Stocks ( 2 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 15 )|
(Schalet, 1986, )
|Secondary FlyBase IDs|
|References ( 43 )|
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|Recent research papers (0)|
|All research papers listed in FlyBase were published before 2011|