G30852768A
G454A
C34Y | tll-PA
C34Y
Polytene chromosomes normal.
Amino acid replacement: C34Y. Nucleotide substitution: TGC to TAC. Residue is present in the first zinc finger.
Point mutation.
MARCM clones of tll1 in the third instar mushroom bodies show a reduction in the number of labelled neurons to 17.2, compared to 200 in controls.
The hindgut of stage 15-16 mutant embryos is severely reduced, but endodermal parts of the midgut are covered with a thin sheet of visceral muscles.
The caudal visceral mesoderm primordium is missing.
Embryos usually lack abdominal segment 8 and have little or no hindgut.
The hindgut is reduced and Malpighian tubules are missing in stage 14/15 embryos.
Strong tll allele.
Initial pattern of prd expression in the embryo drastically altered.
Embryonic defects cannot be suppressed by Dsor1Su1.
Disruption in gt expression patterns: the posterior domain extends posteriorly.
Does not interact with RpII140wimp maternal effect.
Suppression of tor13D embryos: increase in proportion of embryos that formed cuticle with denticles and decrease in proportion of embryos that formed empty sacs.
Homozygous embryos lack the most anterior and posterior structures; the head skeleton is smaller than normal and the Filzkorper, anal plate and spiracles are missing.
Filzkorper, posterior spiracles, anal tufts and anal pads are missing, anterior structures are indistinguishable from tll amorphic embryos. Small increase in segment length.
tll1 embryos have defects in the head skeleton, although the labrum is present. The Malpighian tubules, anal pads and segment A8 are missing. The posterior midgut, proctodeum and pole cells are normal.
Embryos transheterozygous for tll1 and either tlla, tllc or tlle have shortened pharyngeal ridges. A8 and the telson are missing. Homozygous tll1 embryos have no Malpighian tubules, but have a continuous gut that terminates at a clearly formed proctodeal opening at the dorsal posterior tip of the most posterior body segment (A7). One tracheal pit is missing, and the remaining pits appear more widely spaced on the dorsal side of the embryo than in wild-type. The main tracheal trunk ends abruptly at A6. Mature hemizygous tll1 embryos are of normal overall body length, due to an increase in the length of the abdominal segments that are present - this increase in segment length is seen as anteriorly as A2 and is most pronounced in A4, A5, A6 and A7 (becoming more pronounced more posteriorly).
embryonic lethal zygotic lethal with pattern deletions in anterior and posterior of embryo (but body of normal length due to increase in length of non-deleted pattern elements). Anteriorly, dorsal portion of cephalopharyngeal skeleton is defective (dorsal arms shortened, dorsal bridge unfused), dorsal pouch shortened and scleritized, much of brain missing. Posteriorly, eighth abdominal segment and telson, Malpighian tubules, hindgut and much of posterior midgut missing.
fkh1, hb4, kni10, tll1 has cell polarity defective | gastrula stage phenotype
svp1, tll1 has visible | somatic clone phenotype
tll1 is an enhancer of wing vein | ectopic phenotype of Scer\GAL432B, rlSem.C.UAS
tll1 is a suppressor | maternal effect of embryonic/first instar larval cuticle | maternal effect phenotype of tor12D
svp1, tll1 has wing vein | cell autonomous | ectopic | somatic clone phenotype
svp1, tll1 has wing | somatic clone | cell autonomous phenotype
tll1 is rescued by Scer\GAL4elav-C155/tllUAS.cKa
The expression pattern of a variety of homeotic, pair-rule and gap genes in homozygous tll1 mutant embryos has been analysed.
The effects of the tll1 mutation on the spatial expression of hh and wg during embryogenesis have been investigated.
Severity of the embryonic phenotype (deletion of either external structures, A8 or anal pads, or internal structures, hindgut) places tll alleles in the order: Df(3R)tll-pgx > tlll49 > tll1 > tlll29 > tll2 > tllle3.