Numerous genetic screens for maternal effect embryonic lethal mutations resulted in the identification of many genes required for early embryonic polarity. Amongst them, the most important ones are the PAR genes that result in a symmetric first cleavage when knocked out. However, it is still unclear how, for example, the mutual exclusive cortical localisation of the PAR-1/PAR-2 and PAR-3/PAR-6/PKC-3 complexes is initially established at opposite poles of the 1-cell embryo and how the PAR proteins signal to downstream effectors. To identify new genes required for these processes, the phenotypes of 147 chromosome I embryonic lethal loci have been analysed using time-lapse video-microscopy (1). We identified
chp-1 as a gene resulting in a par-like mutant phenotype. It has been shown in plants (barley) that the homologous gene RAR-1 is required for disease resistance (2). CHP-1 contains two zinc-binding domains called CHORD I and CHORD II (cysteine and histidine rich domain). The metazoan versions have a C-terminal extension that shows weak similarity to yeast SGT-1, a supressor of a G2 allele of yeast
skp-1.
chp-1(RNAi) embryos show a symmetric first cleavage, complete or partial rotation of the AB spindle in 90% of the cases, and near-synchronous division of AB and P1. Like in
par-3 or
par-6 mutants, PAR-2 is found all around the cortex of 1 and 2 cell chp- 1(RNAi) embryos. As a consequence, PAR-3 and PAR-6 cortical localisation is reduced. Consistent with CHP-1 being required for embryonic polarity, P-granules are mislocalised at the 4 cell stage. Alongside its role in early embryonic polarity, CHP-1 also plays a role in germline development as
chp-1(RNAi) animals develop a strong sterility phenotype. At the meeting we will present progress on the phenotypic characterisation of
chp-1(RNAi) embryos and discuss possible modes of action.