In a stg2 mutant context, Df(2L)200 mutant embryos induce a twofold increase in the number of crystal cells.
In some segments in mutant embryos tin or eve expressing cells fail to form. Mutants also show severe segmentation and other patterning defects.
Homozygous follicle cell clones have far fewer cells than their wild-type sister clones. The mean ratio of the number of cells in the mutant clone/number of cells in the wild-type sister clone is 0.1 (compared to a ratio of 1.0 in control experiments).
In embryos lacking zygotic stg+, neuroblasts form but arrest at G2 during interphase of cell-cycle stage 14 and fail to enter mitosis.
In homozygous mutant stg2 embryos, single large mononucleated cells with NB6-4 identity are seen in most of the thoracic segments and 90% of abdominal hemisegments. This is in contrast to wild-type where NB6-4T divides into 5 to 6 cells, and NB6-4A divides into 2 cells.
Postblastoderm cell divisions are completely blocked in stg2 mutants. Imaginal disc cells that are homozygous for stg2 divide only once, producing 2-celled clones that are eliminated by cell competition.
Eye of adults heterozygous with stghwy are normal, though missing macrochaetae phenotype remains.
The number of eve-expressing mesodermal cells per hemisegment is similar in stg2 single mutant and stg2; zfh12 double mutant embryos.
Mutant embryos arrest in G2 of cycle 14, while development continues well after the time of mitosis 14. Two centriole pairs are seen per cell. More than 95% of the pairs have incompletely assembled daughters (the daughter centrioles are significantly shorter than their mother centrioles and their tubular fine structure is not obvious).
Cells in homozygous clones induced in the wing pouch of the wing disc divide only once and become enlarged. These cells are gradually lost from the disc epithelium.
All cell divisions are blocked after the blastoderm stage. In embryos sense organ precursors do not divide but do differentiate into neurons, several md but only a few es neurons are observed.
Embryos derived from germ line clones proceed through cycles 1-13 normally and always transverse the maternal/zygotic transition (MZT) during interphase.
Expression of dapGMR.PdN transgene in stg2 flies has no effect on the eye phenotype.
Neuroblast formation occurs normally in stg mutant embryos.
Malpighian tubule phenotype examined in embryos and found to be similar to that of wg mutants: tubules remain as clusters of approximately 20 cells. However in stg2 all four primordia appear. Tip cells are present and tubules go on to elongate and produce uric acid.
No mitoses after mitosis 13 but individuals still develop to secrete a cuticle that is virtually devoid of differentiated pattern elements. Failure of head involution, few thoracic or abdominal denticles develop and tail structures are rudimentary. Introduction of the stghs.PE2 construct without heat shock causes differentiation of more cuticular structure due to leaky expression. Heat shock 2 hours after egg deposition synchronous cell divisions that bore no resemblance to the normal mitotic pattern. Greater number of heat pulses increased the extent of normal cuticle differentiation, 3 pulses gave normal cuticle. These embryos do not hatch as the there are too few CNS cells.
No cell division occurs in the ectoderm after the blastoderm stage in homozygotes.
stg2 embryos first deviate from normal development during the early stages of gastrulation, when they fail to initiate the 14th mitosis. There is no evidence of chromosome condensation, nuclear envelope breakdown or spindle formation between 3 and 12 hours after egg deposition (at 25oC), in contrast to wild type embryos. The cells are arrested in G2. Mutants show a nonspecific reduction in the number of differentiated cuticular structures.