C. elegans embryogenesis begins with a stereotyped sequence of asymmetric cell divisions that are largely responsible for establishing the nematode body plan. These early asymmetries are specified after fertilization by the widely conserved, cortically enriched PAR and PKC-3 proteins, which include three kinases and two PDZ domain proteins. During asymmetric cell divisions in the early embryo, centrosome pairs initially are positioned on transverse axes but then rotate to align with the anteroposterior embryonic axis. We show that rotation of the centrosomal/nuclear complex in an embryonic cell called P1 requires a maternally expressed gene we name spn-4. The predicted SPN-4 protein contains a single RNA recognition motif (RRM), and belongs to a small subfamily of RRM proteins that includes one Drosophila and two human family members. Remarkably, in mutant embryos lacking spn-4 function the transversely oriented ‘P1’ mitotic spindle appears to re-specify the axis of cell polarity, and the division remains asymmetric. spn-4 also is required for other developmental processes, including the specification of mesendoderm, the restriction of mesectoderm fate to P1 descendants, and germline quiescence during embryogenesis. We suggest that SPN-4 post-transcriptionally regulates the expression of multiple developmental regulators. Such SPN-4 targets might then act more specifically to generate a subset of the anterior-posterior asymmetries initially specified after fertilization by the more generally required PAR and PKC-3 proteins.
The maternal gene spn-4 encodes a predicted RRM protein required for mitotic spindle orientation and cell fate patterning in early C. elegans embryos
José-Eduardo Gomes, Sandra E. Encalada, Kathryn A. Swan, Christopher A. Shelton, J. Clayton Carter, Bruce Bowerman; The maternal gene spn-4 encodes a predicted RRM protein required for mitotic spindle orientation and cell fate patterning in early C. elegans embryos. Development 1 November 2001; 128 (21): 4301–4314. doi: https://doi.org/10.1242/dev.128.21.4301
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