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.

(Kurusu et al., 2009)

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.

(Wolfstetter et al., 2009)

The caudal visceral mesoderm primordium is missing.

(Kusch and Reuter, 1999)

hkb² tll¹ double mutant embryos show twisted gastrulation.

(Yip et al., 1997)

Embryos usually lack abdominal segment 8 and have little or no hindgut.

(Diaz et al., 1996)

The hindgut is reduced and Malpighian tubules are missing in stage 14/15 embryos.

(Harbecke and Lengyel, 1995)

Strong tll allele.

(Margolis et al., 1995)

Homozygous tll¹ embryos from rl^Sem/+ mothers have a tll mutant phenotype.

(Brunner et al., 1994)

Initial pattern of prd expression in the embryo drastically altered.

(Gutjahr et al., 1993)

Embryonic defects cannot be suppressed by Dsor1^Su1.

(Tsuda et al., 1993)

Disruption in gt expression patterns: the posterior domain extends posteriorly.

(Kraut and Levine, 1991)

Does not interact with RpII140^wimp maternal effect.

(Parkhurst and Ish-Horowicz, 1991)

Suppression of tor^13D embryos: increase in proportion of embryos that formed cuticle with denticles and decrease in proportion of embryos that formed empty sacs.

(Strecker et al., 1991)

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.

(Lehmann, 1988)

Filzkorper, posterior spiracles, anal tufts and anal pads are missing, anterior structures are indistinguishable from tll amorphic embryos. Small increase in segment length.

(Strecker et al., 1988)

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.

(Tearle and Nusslein-Volhard, 1987)

Embryos transheterozygous for tll¹ and either tll^a, tll^c or tll^e 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).

(Strecker et al., 1986)

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

(Zallen and Wieschaus, 2004)

svp¹, tll¹ has visible | somatic clone phenotype

(Gritzan et al., 2002)

svp¹, tll¹ has wing vein | cell autonomous | ectopic | somatic clone phenotype

(Gritzan et al., 2002)

svp¹, tll¹ has wing | somatic clone | cell autonomous phenotype

(Gritzan et al., 2002)

bcd⁶, nos^L7, tll¹ has epidermis phenotype

(Lehmann and Frohnhofer, 1989)

bcd⁶, nos^L7, tll¹ has telson phenotype

(Lehmann and Frohnhofer, 1989)