Amino acid replacement: R209W.
Nucleotide substitution: A?T.
A8301949T
A?T
R209W | wol-PA
R209W
Homozygous or wol1/Df(2L)BSC111 larvae hatch and have a wild type cuticle by light microscopy. They eventually die after one moult without displaying any obvious phenotype.
Removal of maternal wol in wol1 germline clones results in larvae with patterning and morphological defects, the most prominent being the failure to form a normal head skeleton. The cuticle is discontinuous and the body contours are irregular. At the edges of ruptures, the cuticle is often melanized. Specialized cuticle structures such as denticles are present.
Removal of maternal and zygotic wol in wol1 germline clones causes additional reduction in cuticle deposition and a complete failure of denticle formation and melanization. There is a loss of chitin orientation in the procuticle and dislocation of proteins between epicuticle layers. In the most severe cases, these larvae have an expanded and spongy extracellular matrix beneath the envelope.
Occasionally, in larvae lacking maternal wol from wol1 germline clones, a normal layered cuticle is separated from the surface of the epidermis by an amorphous chitinous matrix. The apical plasma membrane of these cells protrudes ectopic structures into the extracellular space whereas the wild type apical membrane is smooth.
At embryonic stage 17, the apical plasma membrane of wild type and wol1 maternal mutant embryos elaborates the regular arrangement of the so-called apical undulate. In contrast, the apical undulate of wol1 maternal and zygotic mutant embryos appears less regular.
The arrangement of midgut microvilli and hindgut apical plasma membrane seems normal in wol1 maternal mutant larvae. In contrast, midgut microvilli are separated from each other by large gaps and the apical plasma membrane is highly irregular in wol1 maternal and zygotic mutant larvae.
The lateral plasma membrane of epidermal cells fails to extend and the arrangement of septate junctions is disordered in wol1 maternal and zygotic mutant larvae.
The endoplasmic reticulum (ER) of epidermal cells in stage 16 wol1 maternal and zygotic mutant embryos has rather smooth tubules in contrast to the slightly cystic tubules of wild type ER.
Embryos derived from females carrying homozygous germline clones have segmentation defects in the posterior half of the embryo, and a curled-up phenotype resulting from defects in germband elongation and retraction.
Embryos that lack maternal wol function (derived from females carrying homozygous germ line clones) show deletions of alternating abdominal ventral denticle belts, and have a short head and Filzkorper. Embryos that lack both maternal and zygotic wol function (derived from females carrying homozygous germ line clones mated to mutant males) have more severe defects and cuticle holes.
gnyf04215, wol1 has embryonic/first instar larval cuticle | germline clone phenotype
gnyf04215, wol1 has cephalopharyngeal skeleton | germline clone phenotype
gnyf04215, wol1 has denticle | germline clone phenotype