Mutant egg chambers have extremely large ring canals.

Embryos with both maternal and zygotic pcs^gs show defects in early mesodermal patterning and show a "twisted phenotype". At stage 11, there are defects in founder cell specification and there is a concomitant muscle loss in the final muscle pattern. One third of embryos show a severe muscle phenotype including the absence of many muscles with unfused myoblasts present where a muscle should be located. Of the muscles that are present, morphology is defective as they are often not the correct size, shape and orientation and are attached incorrectly to the overlaying epidermis. Posterior segments are most often affected. The remaining two thirds of embryos display only mild to moderate defects in the final muscle pattern.

The maternal/zygotic pcs^gs embryos show defects in mesodermal tissues other than body wall muscles. Marker staining reveals a loss of the visceral and cardiac mesoderm. There is also a loss of neurons in the ventral nerve cord.

Embryos with only maternal copies of pcs^gs show the same "twisted phenotype" as maternal/zygotic pcs^gs embryos. The maternal embryos also show variable defects in the final muscle pattern including muscle loss, unfused myoblasts and defects in muscle morphology. The posterior segments are most severely affected but anterior segments also show muscle patterning defects. In addition to the global mesodermal patterning defects, these embryos display segment-specific defects where one segment contains a more severe muscle phenotype than its adjacent segments. Furthermore, losses of founder cells and neurons can be observed in a segment-specific manner.

Embryos that have zygotic copies of pcs^gs but have the maternal contribution of pcs do not show the posterior patterning defects seen in mutants with maternal pcs^gs. The early mesoderm appears to be specified correctly and visceral and cardiac mesoderm formation appears normal. However, the specification of founder cells is defective and embryos show muscle defects later on including the loss of VO6, VL3 and DA1 muscles and defects in muscle morphology.

Homozygous males have no visible defects in their genitalia.

Homozygous females mated to wild-type males give rise to 70% agametic adult progeny (an incompletely penetrant grandchildless phenotype). In 10% of the progeny, mosaic pairs of gonads are seen, where only one ovary or testis is agametic. 70% of embryos derived from homozygous females have a dramatically reduced number or completely lack germ cells. At 18^oC, 5% of embryos derived from homozygous females mated to wild-type males show a variable but characteristic abdomenless phenotype and 85% of the adults that develop from the embryos have a grandchildless phenotype. The progeny of homozygous females mated to homozygous males show abdominal defects characteristic of posterior group mutations, coupled with holes in the cuticle that are most frequently seen in the head region.

pcs^gs has grandchildless phenotype, suppressible by Btk^k00206

pcs^gs has grandchildless phenotype, suppressible by Btk^unspecified/Btk^k00206

pcs^gs has grandchildless phenotype, suppressible by Btk^k05610/Btk^fic-P

pcs^gs has grandchildless phenotype, suppressible by Btk^fic-P/Btk^fic-P

pcs^gs has nurse cell ring canal phenotype, suppressible by Btk^fic-P

pcs^gs has embryonic segment | maternal effect phenotype, suppressible by Btk^k00206

pcs^gs is a suppressor of nurse cell ring canal phenotype of Btk^fic-P

pcs^gs is a suppressor of phallapodeme phenotype of Btk^fic-P