shgg317 mutant embryos display defects in the actin dynamics in the amnioserosa cells compared to controls.
In embryos from females heterozygous for shgg317, an average of 3.7 PGCs are left outside the midgut with 64% of embryos exhibiting a phenotype.
In shgg317 homozygous embryos gonad compaction is sometimes initiated, but often does not proceed to completion. The three clusters of somatic gonadal precursors (SGPs) from parasegments (PS) 10-12 are able to associate correctly with one another, and with germ cells, to form a cohesive group. However, these cells often remain loosely associated and spread over more than one parasegment, rather than compacting tightly in PS10. In the most severe cases, compaction from PS10-12 to PS10 appears completely blocked. In weaker examples, compaction is initiated but not completed, resulting in partially compacted and misshapen gonads. During ensheathment of germ cells by gonadal mesoderm in these embryos the gonadal mesoderm cells fail to make cellular extensions between and around the germ cells. Phenotypes are stronger in these embryos than in shg2 homozygotes. This is true, both for the compaction phenotype (22% severe, 41% weak, n=49 in shgg317 homozygotes; 3% severe, 50% weak, n=36 in shg2 homozygotes) and the ensheathment phenotype, but the severity of these two phenotypes do not correlate with each other. In male shgg317 homozygous embryos male specific gonadal precursors often fail to join the posterior of the male gonad (42% male embryos n=49). Offspring from heterozygous shgg317/+ females are viable, but the embryos have a significant germ cell migration defect. Offspring from the reciprocal cross using shgg317/+ males show no germ cell migration defect.
Class IV allele: mutants lack all head and ventral cuticle, and show segmental defects in lateral epidermis or dorsal and lateral epidermis. Defects are evident in the neurectoderm, Malpighian tubules, optic lobe precursor, PNS and SNS. In germ-line clones, no eggs are recovered.
The principal midgut epithelial cells spread over the visceral mesoderm but do not become columnar, they maintain a rounded to cuboidal shape, and do not form a monolayer. At later stages (stage 14-17) the principle midgut epithelial cells become attached to the visceral mesoderm and gradually adopt a more wild type appearance. By the time the embryos are fully differentiated, no difference from wild type can be seen.
shgg317 has abnormal cell migration | maternal effect phenotype, enhanceable by Jafrac1[+]/Prx2KG05372
shgg317 has abnormal cell adhesion | maternal effect phenotype, enhanceable by Jafrac1[+]/Prx2KG05372
shgg317 has germline cell | maternal effect phenotype, enhanceable by Jafrac1[+]/Prx2KG05372
shgg317 has neurogenic region phenotype, suppressible by Nint.hs
shgg317 has Malpighian tubule phenotype, suppressible by ctC145
shg[+]/shgg317 is an enhancer of germline cell | embryonic stage 15 phenotype of raw155.27/raw134.47
shgg317 is an enhancer of germline cell | embryonic stage 15 phenotype of raw155.27/raw134.47
shg[+]/shgg317 is an enhancer of adult thorax phenotype of Src42A6-1
ena[+]/enaC14-06, shgg317 has gonad | embryonic stage phenotype
enaC14-06, shg[+]/shgg317 has gonad | embryonic stage phenotype
Embryos from Jafrac1KG05372, shgg317 trans-heterozygous mothers display a significantly enhanced primordial germline cell adherence defect compared to single shgg317 mutants. These mothers produce embryos with an average of 6.2 primordial germline cells left outside of the midgut with 91% of embryos affected.
Df(2R)E2/shgg317 is rescued by shgUbi-p63E.sgGFP
Strong allele. Visceral mesoderm develops normally.