There are no hematopoietic cells in the lymph gland of zfh12 mutant embryos.
zfh12/Df(3R)GC14 mutant embryos exhibit severe disruption to somatic muscle patterning, with little apparent organisation of muscles in the ventral and lateral regions.
Mutant embryos lack the eve-positive pericardial cells from the linear heart tube. The cardiac myocytes are present in the normal number, but they are abnormally aligned, resulting in a distorted heart tube.
Early steps in mesoderm differentiation, such as the formation of somatic, visceral and cardiac mesoderm appears normal in zfh12 embryos. The eve-expressing pericardial cells (EPCs) are missing. The majority of the myocardial and the pericardial cells are present in later embryos, but the heart structure has minor to moderate defects. Some of the body wall muscles are defective or missing.
Embryonic cuticle normal. Somatic musculature shows variable patterning and insertion site positioning defects, principally in the ventral oblique and the dorsal muscles. These pattern defects are evident at the segregation of the muscle precursors, as revealed by an aberrant pattern of S59 gene expression. Midgut development is abnormal: constrictions rarely complete the subdivision of the yolk. Variable heart defects are evident as kinked or discontinuous heart. Examination with antibody to the vasa gene product pole cell marker reveal that the shape of the gonads is also abnormal. The adult muscle precursors in the embryo, identified as persistant twist-expressing cells, show variable abnormalities of number and position: up to 25% of the adult muscle precursor cells can be missing.
zfh12 has embryonic/larval pericardial cell phenotype, suppressible by Scer\GAL4twi.PG/Scer\GAL4how-24B
zfh12 has cardioblast phenotype, suppressible by Scer\GAL4twi.PG/Scer\GAL4how-24B
zfh12 has embryonic/larval dorsal vessel phenotype, suppressible by Scer\GAL4twi.PG/Scer\GAL4how-24B
zfh12 has pericardial cell phenotype, suppressible by Scer\GAL4twi.PG/eveUAS.cBa
zfh12 has embryonic/larval lymph gland | embryonic stage phenotype, non-suppressible by dppd6
zfh12 has hemocyte | embryonic stage phenotype, non-suppressible by dppd6
The number of eve-expressing mesodermal cells per hemisegment is similar in stg2 single mutant and stg2; zfh12 double mutant embryos. numb2 ; zfh12 double mutant embryos have no eve-expressing pericardial cells (EPCs) and no DA1 muscles, except for rarely 1 or 2 EPCs are present. spi1 ; zfh12 embryos have no EPCs and no DA1 muscles. Ectopic expression of eveScer\UAS.cBa under the control of Scer\GAL4twi.PG in a zfh12 background restores the formation of some EPCs.
zfh12 is rescued by Scer\GAL4how-24B/zfh1UAS.cPa
zfh12 is rescued by Scer\GAL4twi.PG/Scer\GAL4how-24B/zfh1UAS.cLb
Expression of zfh1Scer\UAS.cPa under the control of the pan-mesodermal driver Scer\GAL4how-24B in zfh12 mutants rescues the lymph gland phenotype.
Identification of zfh1 alleles rests on several alleles of this complementation group having no detectable zfh1 protein. Phenotype of zfh12 over deficiciency for zfh1 not described.