Chondroitin acts in the guidance of gonadal distal tip cells in C. elegans

In Caenorhabditis elegans hermaphrodites, the U-shaped gonad arms are formed by directed migration of the gonadal distal tip cells (DTCs). The stereotyped pattern of DTC migration is carefully controlled by extracellular and cell surface molecules during larval development. Here we report that two p...

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Bibliographic Details
Published in:Developmental biology 2006-12, Vol.300 (2), p.635-646
Main Authors: Suzuki, Norio, Toyoda, Hidenao, Sano, Mitsue, Nishiwaki, Kiyoji
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Animals
Caenorhabditis elegans - embryology
Caenorhabditis elegans - genetics
Caenorhabditis elegans - metabolism
Caenorhabditis elegans Proteins - genetics
Cell migration
Cell Movement - genetics
Cell Movement - physiology
Chondroitin - physiology
Chondroitin polymerizing factor
Chondroitin synthase
Female
Glycosyltransferases - genetics
Male
Molecular Sequence Data
Ovary - cytology
Ovary - embryology
Ovary - metabolism
Testis - cytology
Testis - embryology
Testis - metabolism
UNC-6/netrin guidance
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Summary:In Caenorhabditis elegans hermaphrodites, the U-shaped gonad arms are formed by directed migration of the gonadal distal tip cells (DTCs). The stereotyped pattern of DTC migration is carefully controlled by extracellular and cell surface molecules during larval development. Here we report that two proteins, SQV-5 (chondroitin synthase) and its cofactor MIG-22 (chondroitin polymerizing factor), are required for chondroitin biosynthesis and are essential for the dorsally guided migration of DTCs. We found that MIG-22 is expressed in migrating DTCs, hypodermal seam cells, developing vulva and oocytes. The expression of SQV-5 or MIG-22 in both DTCs and hypodermis rescued the DTC migration defects of the relevant mutants more efficiently than when they were expressed in either single tissue. Furthermore, the expression of SQV-5 by the mig-22 promoter significantly rescued sqv-5 mutants, implying that these two proteins act in the same tissues and that chondroitin proteoglycans produced in both of these tissues are required for DTC migration. The DTC migration defects caused by sqv-5 or mig-22 mutations were partially suppressed in the anterior and enhanced in the posterior DTCs in unc-6, unc-5 or unc-40 mutant backgrounds, suggesting that chondroitin proteoglycans play roles in the UNC-6/netrin-dependent guidance of DTCs.
ISSN:0012-1606
1095-564X
DOI:10.1016/j.ydbio.2006.08.037