prcMB03017 homozygotes, prc3-21/prcMB03017 and prc3-548/prcMB03017 larvae have a cardiac phenotype consisting of detached pericardial cells, severely misguided myofibers and severe heart tube luminal collapse resulting in a significantly reduced heart diameter.
In homozygous prcMB03017 mutant larvae the pericardial cells irreversibly detach from the heart tube, with the phenotype becoming fully visible at the third instar larval stage. Viability is not affected and the defect can also be detected in pharate adults. There is no effect on fertility. Determination and migration of heart precursor cells is unaffected.
prcMB03017/Df(3L)vin6 mutant third instar larvae show a strong detachment of pericardial cells from the heart tube. The detachment of the pericardial cells also ruptures the connection between the alary muscles and cardiomyocytes. Furthermore, the morphology of the cardiomyocytes itself is dramatically altered in prcMB03017/Df(3L)vin6 mutants, with the cells exhibiting an uncoordinated distribution of actin fibers and an altered cell shape.
The beating pattern of the heart is dramatically altered in prcMB03017/Df(3L)vin6 mutant third instar larvae. A changed contraction movement of the whole organ is observed along the posterior-anterior axis. No systole or diastole are detectable.
Homozygous prcMB03017 mutant third instar larvae exhibit severe defects in heart function. In contrast to wild type flies, prcMB03017 mutant flies fail to accumulate dye in the head after injection of a fluorescent tracer into the abdomen.
The average lifespan of homozygous prcMB03017 mutant flies is decreased by 46% compared to controls.
As in wild type, the cardiomyocytes in prcMB03017 mutant embryos are localised along the dorsal midline at the end of embryogenesis (stage 17), showing that dorsal closure is unaffected. However, frequently the cardiomyocytes in homozygous prcMB03017 mutants fail to seal the lumen properly at the ventral side of the heart tube. In wild type flies the luminal and basal membranes of the cardiomyocytes are covered by a distinct basement membrane and this is not significantly altered in prcMB03017 mutants. Although the pericardial cells are not fully detached from the embryonic heart, but small gaps are seen between the cells and rupture of the connecting ECM is detectable.
prcMB03017/prc3-548 is rescued by prc+t32
prcMB03017 is rescued by prc+t32
prcMB03017/prc3-21 is partially rescued by prc+t32
prcMB03017/prc3-21 is not rescued by prcfTRG00497.sfGFP-TVPTBF
prcMB03017/prc3-548 is not rescued by prcfTRG00497.sfGFP-TVPTBF
prcMB03017 is not rescued by prcfTRG00497.sfGFP-TVPTBF
prc+t32 fully rescues the dissociation of pericardial cells from the heart both in prcMB03017 homozygous and prc3-548/prcMB03017 transheterozygous larvae. This cardiac phenotype is only partially rescued in prc3-21/prcMB03017 transheterozygotes.