Point mutant.
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.
Eye of adults heterozygous with stghwy are normal, though missing macrochaetae phenotype remains.
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.
Cell division arrested.
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.
strong allele
stg2 is an enhancer of visible phenotype of Scer\GAL4en-e16E, armUAS.cWa
stg2 is a non-enhancer of visible phenotype of DpGMR.PD, E2f1GMR.PD
stg2/stg[+] is a suppressor of increased cell death phenotype of shtd1
stg2 is a suppressor of visible phenotype of Scer\GAL4en-e16E, shgi.UAS.Tag:SS(aos),Tag:MYC
stg2 is a non-suppressor of visible phenotype of DpGMR.PD, E2f1GMR.PD
stg2, twe1 has decreased cell number | oogenesis phenotype
stg2, twe1 has decreased occurrence of cell division | oogenesis phenotype
stg2 is an enhancer of wing margin bristle | ectopic phenotype of Scer\GAL4en-e16E, armUAS.cWa
stg2 is an enhancer of wing phenotype of Scer\GAL4en-e16E, armUAS.cWa
stg2 is a non-enhancer of phenotype of Mybunspecified
stg2/stg[+] is a suppressor of ommatidium phenotype of shtd1
stg2 is a suppressor of wing phenotype of Scer\GAL4en-e16E, shgi.UAS.Tag:SS(aos),Tag:MYC
stg2 is a non-suppressor of phenotype of Mybunspecified
stg2/stg[+] is a non-suppressor of lamina anlage & mitotic cell cycle phenotype of dally06464
stg2, twe1 has female germline cell | oogenesis phenotype
The addition of stg2 has no effect on Mybunspecified viability.
One copy of stg2 does not rescue the second division in dally06464 lamina precursor neurons and appears to expand the first G2/M domain of lamina precursor neuron division.
In stg2/stg4,Df(3L)ri-79c double mutant embryos no post-blastoderm cell divisions occur and gastrulation is normal.
The cell division phenotype is partially rescued by stgt31.6; cell cycle progression is seen in a subset of the wild-type division pattern, and the embryos die with mild cuticular defects which can be attributed to a partial loss of cell division in mitotic domain 11 (the dorsolateral epidermis). The imaginal disc phenotype is rescued by stgt31.6, stgBCD, stgCD or stgt6.0; stg2 cells in the imaginal disc carrying one of these transgenes divide many times and produce large clones of cells. stg2 clones rescued by stgt31.6 are equal in size to their wild-type sister clones, while stg2 clones rescued by any of the other transgenes are smaller than their wild-type sister clones and show increased cell size. stg2 cells rescued by stgt6.0 have an increased G2 phase.
Strong stg allele.