The Caenorhabditis elegans par-5 Gene Encodes a 14-3-3 Protein Required for Cellular Asymmetry in the Early Embryo

Abstract

The establishment of anterior-posterior polarity in the Caenorhabditis elegans embryo requires the activity of the maternally expressed par genes. We report the identification and analysis of a new par gene, par-5. We show that par-5 is required for asynchrony and asymmetry in the first embryonic cell divisions, normal pseudocleavage, normal cleavage spindle orientation at the two-cell stage, and localization of P granules and MEX-5 during the first and subsequent cell cycles. Furthermore, par-5 activity is required in the first cell cycle for the asymmetric cortical localization of PAR-1 and PAR-2 to the posterior, and PAR-3, PAR-6, and PKC-3 to the anterior. When PAR-5 is reduced by mutation or by RNA interference, these proteins spread around the cortex of the one-cell embryo and partially overlap. We have shown by sequence analysis of par-5 mutants and by RNA interference that the par-5 gene is the same as the ftt-1 gene, and encodes a 14-3-3 protein. The PAR-5 14-3-3 protein is present in gonads, oocytes, and early embryos, but is not asymmetrically distributed. Our analysis indicates that the par-5 14-3-3 gene plays a crucial role in the early events leading to polarization of the C. elegans zygote.

A Genomewide RNAi Screen for Genes That Affect the Stability, Distribution and Function of P Granules in Caenorhabditis elegans

“…This pattern likely reflects both missegregation of P granules and failure to properly separate germ-line and somatic lineages, with their different abilities to retain (germ-line) vs. disassemble (somatic) P granules (Kemphues et al 1988). As exemplified by let-99, par-5, and cdc-25.1, RNAi depletion caused PGL-1 to be present in all cells of early embryos and to persist in numerous cells of later embryos (Rose and Kemphues 1998;Morton et al 2002). We suspect that the extra PGL-1-containing cells in later embryos are in most cases a consequence of the Cell cycle/polarity/cell division(C) air-1, bir-1, cdc-25.1, cdc-42, cdk-1, cdk-9, cyk-4, dhc-1, dnc-1, dom-6, egg-3, gsk-3, ify-1, let-99, mbk-2, nmy-2, par-1, par-2, par-5, par-6, plk-1, spd-5, sqv-6, tbb-2, tbg-1, zen-4, zyg-9, F22B5.10…”

AMPK blocks starvation-inducible transgenerational defects in Caenorhabditis elegans

“…If AMPK-dependent phosphorylation of SET-2 or other components of the COMPASS complex results in recognition of the phosphotargets by 14-3-3 proteins to mediate its effects downstream of nutrient/energy stress, then loss of the C. elegans 14-3-3 proteins should recapitulate the phenotypes typical of AMPK compromise in post-L1 diapause animals. In C. elegans there are two predicted 14-3-3 proteins: ftt-2 and par-5, but only par-5 is expressed in the germ line (42,43). Because par-5 is an essential gene we performed RNA soaking experiments with dsRNA corresponding to par-5 during the L1 diapause.…”

Mécanismes de division cellulaire asymétrique

“…Après la fécondation, un (ou plusieurs) facteur(s) véhicu-lés par le spermatozoïde inhibe(nt) localement les contractions corticales du cytosquelette d'actine qui vont se déplacer vers le pôle antérieur et circonscrire alors deux domaines corticaux distincts [3] : PAR-6 et PAR-3 forment un complexe avec la protéine kinase PKC-3 au cortex antérieur, tandis que PAR-1 et PAR-2 sont restreintes au cortex postérieur ( Figure 1B). PAR-4 et PAR-5 restent distribuées de façon symétrique sur l'ensemble du cortex ainsi que dans le cytoplasme et permettent de définir et de stabiliser la limite entre les domaines antéro-postérieurs [4,5]. La mise en place et le maintien des deux domaines corticaux distincts : PAR-3/PAR-6/PKC-3 au cortex antérieur et PAR-1/PAR-2 au cortex postérieur, reposent sur une inhibition réciproque des deux complexes l'un vis-à-vis de l'autre ( Figure 1C).…”