mutant embryos show cardioblast (CB) patterning defects and significantly fewer cardioblasts, specifically generic cardioblasts leading to lower generic CBs:ostial CBs ratio than the typical 4:2 ratio. These embryos also exhibit a significant decrease in the number of odd pericardial cells, although even pericardial cells are unaffected, as compared to controls.
The concentration of circulating hemocytes in spi1
heterozygous third instar larvae is comparable to that in wild-type controls.
/+ heterozygotes display normal patterning and cell numbers in pupal retina.
mutant embryos exhibit defects in ventral patterning. The denticle belts are narrow and some are fused.
Small clones of spi1
glial cells recovered using MARCM show no effect in the underlying larval neuroepithelium or in the final optic lobe size.
Mutant embryos show a decrease in the number of dorsolateral and lateral adult muscle precursor cells compared to wild type.
Flies heterozygous for spi1
have normal cardiac function.
The proliferation of spi1
mutant clones of adult midgut progenitor cells is normal.
Eggs derived from egg chambers containing complete homozygous follicle cell clones appear normal and have two dorsal appendages.
Clones in third instar eye discs do not show defects in R8 spacing or cell clustering behind the furrow. Only slightly elevated levels of cell death are observed.
Minute clones in the eye disc do not affect the formation of rosettes and arcs of cells in the morphogenetic furrow.
embryos, apoptosis is induced throughout the cells of the posterior compartment.
Homozygous embryos have a reduced number of midline glia per ventral nerve cord segment compared to wild type.
94% of cuticles from spi1
homozygous embryos show fusion of at least one pair of denticle belts, with the majority having between 1 and 3 fusions. During stages 10-14, embryos of this genotype have increased levels of apoptosis in epidermis around the ventral midline.
No increase is seen in cardioblast numbers in the developing embryo.
Metameric furrow form and are maintained normally in spi1
mutant embryos, sensory axons project abnormally across segment boundaries and glial morphology is abnormal. Additionally, the anterior and posterior sensory fascicles are spaced further apart at the CNS-PNS transition zone compared to wild type.
The number of midline glial cells in spi1
homozygous stage 17 embryos is greatly reduced compared to wild-type.
Homozygous clones in the adult abdomen do not show any consistent alterations of normal polarity.
Homozygous somatic clones in the legs and wings have bractless mechanosensory bristles.
Border cells still migrate dorsally when all dorsal follicle cells are mutant for spi1
in females containing homozygous clones.
The number of chordotonal organs in the lateral cluster is reduced from 5 to 3 in stage 16 homozygous embryos and there is a complete lack of oenocytes. Oenocyte precursor whorls are missing in stage 11 embryos.
The number of neurons in the lch5 organ is reduced from five to three in mutant embryos. Late stage embryos show a loss of oenocytes.
2.4 +/- 0.4 midline glia (MG) are seen per segment in stage 12/0 mutant embryos (wild-type embryos have 5.6 +/- 0.2 MG cells per segment at this stage). At stage 17 mutant embryos have 1.9 +/- 0.8 MG per segment compared to the wild type 3.0 +/- 0.1 MG per segment. The number of midline cells in the dorsal nerve cord is reduced in mutant stage 16 embryos, while the ventral cell number and position are unaffected. Thickening and fusion of the commissures and thinning of the longitudinal tracts is seen.
somatic clones in the eye disc, the amount of apoptosis seen is slightly above that seen in wild-type.
The Bolwig's organ is smaller than normal in mutant embryos. The posterior lip of the optic lobe is reduced in size.
clones in the wing have no effect on vein patterning.
Homozygous embryos lack approximately half of the normal myofibres; gaps are present in the set of ventral longitudinal muscles and only one of the normal 3 ventral oblique muscles is present, although all lateral transverse muscles develop normally. The precursor of muscle DA1 is missing. Muscles DO1, LT2 and LT4, and the eve
-expressing pericardial cell precursors form normally. The P15 muscle precursor cell does not form. Apoptosis within the mesoderm is significantly higher than in wild-type embryos, and myoblasts engulfed by macrophages are seen.
Embryos show loss of optic lobe and Bolwig's organ and reduction of dorsomedial and ventromedial brain, the stomatogastric nervous system, the hypocerebral ganglion and the recurrent nerve.
double heterozygotes do not have a visible phenotype.
Germline clones fail to rescue the female sterile phenotype of Fs(2)Ugr
Early CNS development is essentially normal in mutant embryos.
hypomorphic females lay eggs that show a significant loss of the most dorsal tissue. Germline clones reveal no requirement for spi
in patterning the egg, or in the viability or patterning of the embryo.
In homozygous larvae the most ventral denticle belts are absent and denticle rows are fused between segments. In spi1
mutants the denticle bands are narrower with some fusion of denticles between segments.
Either no dorsal medial cells or reduced numbers of cells form.
embryos exhibit deletion of ventral denticles so the width of the belt is reduced. Wing, leg, haltere and eye/antenna spi1
mutant discs can be in vivo cultured.
In mutant eye clones the initial single neuron stage ommatidia appear normal, as do their spacing. However no further progression occurs, and the clusters appear to be arrested at the one neuron stage. The wave of DNA synthesis immediately following the furrow is unaffected in spi
mutant clones. The early development of the preclusters is normal up until the 5-cell stage. Development proceeds normally anterior to and in the furrow (up to the specification and early differentiation of the founding R8 photoreceptor cells) but the specification of R2 and R5, and all subsequent steps, fail. Homozygous spi
mutant clones are apparently equal in size to their homozygous wild-type twin-spots.
No effect on the faf
Mitotic clones have reduced numbers of photoreceptors and loss of whole ommatidia.
Retinal clones induced during first larval instar show defects in the formation of photoreceptor cells R8, R2, R5, R3 and R4.
Nondefective in gonad assembly.
Malpighian tubules of homozygous embryos are short and each contains an average of only 39 cells.
All or nearly all of the ventral epidermal cells are absent in mutant embryos.
Salivary placodes are expanded towards the ventral midline.
Epidermal defects and fusion of the anterior and posterior commissures. In the PNS some sensory organs are missing, there is a ventral-dorsal gradient of severity. Several muscle fibres are always missing in the dorsolateral region and there are variable abnormalities in the number, shape and attachment sites of the eight ventral oblique muscle fibres.
Anterior and posterior commissure fuse. Initial development of the axon commissures appears normal but the axon tracts fail to separate at the time of midline glia migration. Midline glial cells are present but fail to migrate.