Homozygous somatic clones in the legs and wings have bractless mechanosensory bristles.
Small clones of cells in the eye disc initiate ectopic photoreceptor differentiation only when they are close to the morphogenetic furrow.
Homozygous embryos exhibit defects in posterior pattern.
Clonal analysis reveals phenotypes in the adult including loss of wing vein, ectopic wing vein, reduced cell size, extra bristles and cell lethality.
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.
tll expression is completely missing posteriorly.
Little or no tll expression is detected in the posterior of syncytial or cellular blastoderm embryos, at the anterior the early tll cap does not appear and an abnormal anterior tll stripe appears by the late syncytial blastoderm.
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.
Lethal phase in homozygotes is at the larval-pupal boundary. The number of larvae that pupate is greater at low temperatures. Imaginal discs of affected homozygotes are rudimentary. The imaginal ring in the salivary gland is reduced. Number of mitotic figures in larval brain squashes is dramatically reduced. Embryos derived from germ line clones display two phenotypes. One half of the embryos (those that are paternally rescued) fail to develop structures posterior to the seventh abdominal segment. They occasionally show head involution defects or U-shaped or twisted development. Cellular blastoderm stage corresponding to these embryos appears basically normal except for a small uncellularised region at the posterior pole, beneath the pole cells. One half of the embryos (those that are not paternally rescued) show a weak disorganised cuticle consisting mostly of dorsal structures. Cellular blastoderm stage corresponding to these embryos shows multiple layers of abnormal nuclei situated along the peripheral cytoplasm. The cytoplasm is distributed unevenly along their surface.
Embryonic lethality is seen in embryos from homozygous phl7 germline.
Raf7 is an enhancer of visible phenotype of Scer\GAL4GMR.PF, btlλ.UAS, stumpsUAS.Tag:FLAG
Raf7 is an enhancer of partially lethal - majority die phenotype of SlikKG04837/Slik1
Raf7 is an enhancer of increased cell death phenotype of SlikKG04837/Slik1
Raf[+]/Raf7 is an enhancer of increased cell death | larval stage | somatic clone phenotype of Slik1
Raf7/phl[+] is a non-enhancer of visible phenotype of Scer\GAL4Tub.PU, cswN308D.UASp
Raf7/phl[+] is a non-suppressor of visible phenotype of Scer\GAL4Tub.PU, cswN308D.UASp
Raf7 is an enhancer of eye phenotype of Scer\GAL4GMR.PF, btlλ.UAS, stumpsUAS.Tag:FLAG
Raf7 is an enhancer of wing phenotype of SlikKG04837/Slik1
Raf7/phl[+] is a non-enhancer of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp
Raf7/phl[+] is a non-suppressor of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp
Raf7 is a non-suppressor of ommatidium phenotype of Rac1V12.hs.sev
Raf7/phl[+], da2 has follicle cell phenotype
Raf7, da2 has follicle cell phenotype
When phl7 is added to slikScer\UAS.cHa, Scer\GAL4ptc-559.1 animals the overgrowth phenotype is completely suppressed. When heterozygous phl7 is added to slik1/slikKG04837 animals about 40% of animals survive(as opposed to 90%) and the penetrance of the wing phenotype is increased from 11% to almost 100%. The number of apoptotic cells seen also increases.
Suppressor of the dosage-dependent (two or more copies of P{sev-svp1} or P{sev-svp2}) transformation of cone cells into R7 photoreceptors and at a lower frequency R7 cells into outer photoreceptors.
Lefevre.
Maternal germline clonal analysis demonstrates there is a maternal effect lethal phenotype, acron and telson are missing.
A strong allele of phl.
Comparison of homozygotes for this allele with heterozygotes for this allele and Df(1)64c18 (deleted for phl) is the basis for amorph designation. Isolation described in Perrimon et al., 1985, Dev. Biol. 110: 480.
Clones induced using X chromosomes with an FRT sequence near the centromere.