The piragua (prg) locus encodes a protein with an amino terminal ZAD (zinc associated domain) and nine C2H2 zinc fingers. It is expressed throughout the life cycle, and is required for embryogenesis and early larval life. A fraction of mutant embryos die during embryogenesis, either with an early phenotype (no cuticle formed), or at the end of embryogenesis with defective cuticles (dorsal closure and head involution defects). Surviving embryos die as first instar larvae. I also found that flower, that codes for a membrane protein, is required for embryogenesis. Two mutants flower alleles examined display late embryonic developmental cuticular phenotypes, of which most are head involution defects. Surviving embryos die as first instar larvae, as do surviving piragua embryos. In a published gain-of-function screen in wing imaginal discs, both genes were isolated by virtue of expression in dying, outcompeted cells, and for both being required for cell death in these cells (Rhiner, et al, 2010). We wondered whether the two loci might genetically interact in the embryo. Genetic experiments show that indeed the two loci interact, as homozygous mutants for one allele while heterozygous for the other show a significant augmentation of embryonic phenotypes. In contrast, mutant eye phenotypes for piragua are at variance from those of mutant flower alleles. piragua mutant eye clones show extensive cellular disarray, picnotic figures, lack of eye bristles, and aberrant cone morphology. This compares to a much less dramatic phenotype of lack of supernumerary cell culling at the eye borders during eye formation, a process that requires flower (Merino, et al 2013). This implies that piragua and flower might have both common and distinct functions.
Funded by CONACYT # 177962.
Bibliography:
Rhiner, et al (2010). Dev. Cell. 18(6): 985--998.
Merino, et al (2013). Curr. Biol. 23(14): 1300--1309.