The maternal gene spn-4 encodes a predicted RRM protein required for mitotic spindle orientation and cell fate patterning in early C. elegans embryos.
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 P(1) 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 'P(1)' 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 P(1) 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.
Gomes
J E
JE
Institute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA.
Encalada
S E
SE
Swan
K A
KA
Shelton
C A
CA
Carter
J C
JC
Bowerman
B
B
D020816:Amino Acid Motifs; D000595:Amino Acid Sequence; D000818:Animals; D017173:Caenorhabditis elegans / Q000196:embryology / Q000235:genetics*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics* / Q000378:metabolism*; D018797:Cell Cycle Proteins / Q000235:genetics* / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000235:genetics; D004625:Embryo, Nonmammalian; D004627:Embryonic Induction; D004707:Endoderm; D005260:Female; D050980:GATA Transcription Factors; D018507:Gene Expression Regulation, Developmental; D018392:Genomic Imprinting; D015801:Helminth Proteins / Q000235:genetics / Q000378:metabolism; D018398:Homeodomain Proteins; D006801:Humans; D008297:Male; D008969:Molecular Sequence Data; D009154:Mutation; D010614:Pharynx / Q000196:embryology; D017346:Protein Serine-Threonine Kinases; D016601:RNA-Binding Proteins / Q000235:genetics* / Q000378:metabolism*; D008941:Spindle Apparatus / Q000502:physiology*; D015534:Trans-Activators; D014157:Transcription Factors / Q000235:genetics
D029742:Caenorhabditis elegans Proteins; D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D050980:GATA Transcription Factors; D015801:Helminth Proteins; D018398:Homeodomain Proteins; C433251:MED-1 protein, C elegans; D016601:RNA-Binding Proteins; C442231:SPN-4 protein, C elegans; D015534:Trans-Activators; D014157:Transcription Factors; C068665:pal-1 protein, C elegans; C073702:skn-1 protein, C elegans; C097238:PAR-3 protein, C elegans; D017346:Protein Serine-Threonine Kinases