Altered expression of an L1-specific, O-linked cuticle surface glycoprotein in mutants of the nematode Caenorhabditis elegans.

Hemmer, Ruth M.; Donkin, Steven G.; Chin, Karl J.; Grenache, David G.; Bhatt, Harshida; Politz, Samuel M.

doi:10.1083/jcb.115.5.1237

Cited by 28 publications

(32 citation statements)

References 30 publications

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“…srf-2 and srf-3 were initially defined by ectopic binding of a polyclonal antibody that failed to bind wildtype adults (Politz et al 1990). Subsequently, a different phenotype was observed in staining with monoclonal antibodies: these reagents recognized an epitope on the surface of wild-type L1 larvae that is absent from srf-2 and srf-3 animals (Hemmer et al 1991). srf-2 and srf-3 worms also are bound ectopically by lectins that do not bind most of the wild-type surface, and this phenotype was used to identify an additional gene, srf-5 (Link et al 1992).…”

Section: Discussionmentioning

confidence: 99%

“…Antibody binding: A published protocol (Hemmer et al 1991) was used with minor modifications. Nematodes were washed three times in phosphate-buffered saline (PBS) and then incubated for 2.5 hr with a 50-fold dilution of monoclonal antibody M37 in PBS.…”

Section: Methodsmentioning

confidence: 99%

“…Stage-specific phenotypes of bah-3 and srf-6 mutants: Antibody M37 binds to L1 larvae but not to other stages of wild-type C. elegans under normal growth conditions (Politz et al 1990;Hemmer et al 1991). Alone among the mutants recovered in the Bah screen, bah-1 and bah-2 had the wild-type antibody phenotype ( Table 2).…”

Section: ; Yook and Hodgkin 2007)mentioning

confidence: 99%

“…Cld was first described for mutations in srf-6 (Hemmer et al 1991;Grenache et al 1996). We tested each stage of srf-6 mutants by growing them synchronously on E. coli OP50 and then transferring them to Y. pseudotuberculosis.…”

Section: ; Yook and Hodgkin 2007)mentioning

confidence: 99%

“…This identified three genes whose mutants appear to have primary defects in the surface: srf-2, srf-3, and srf-5 (Politz et al 1990;Link et al 1992). Mutations in srf-6 result in stage-specific defects in surface antigen display (Hemmer et al 1991;Grenache et al 1996). 1 Additional surface-determining genes were identified using infection by the nematode-specific pathogen Microbacterium nematophilum, which causes anal swelling.…”

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Caenorhabditis elegans Mutants Resistant to Attachment of Yersinia Biofilms

et al. 2007

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The detailed composition and structure of the Caenorhabditis elegans surface are unknown. Previous genetic studies used antibody or lectin binding to identify srf genes that play roles in surface determination. Infection by Microbacterium nematophilum identified bus (bacterially unswollen) genes that also affect surface characteristics. We report that biofilms produced by Yersinia pestis and Y. pseudotuberculosis, which bind the C. elegans surface predominantly on the head, can be used to identify additional surface-determining genes. A screen for C. elegans mutants with a biofilm absent on the head (Bah) phenotype identified three novel genes: bah-1, bah-2, and bah-3. The bah-1 and bah-2 mutants have slightly fragile cuticles but are neither Srf nor Bus, suggesting that they are specific for surface components involved in biofilm attachment. A bah-3 mutant has normal cuticle integrity, but shows a stage-specific Srf phenotype. The screen produced alleles of five known surface genes: srf-2, srf-3, bus-4, bus-12, and bus-17. For the X-linked bus-17, a paternal effect was observed in biofilm assays.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: ; Yook and Hodgkin 2007)mentioning

confidence: 99%

Section: ; Yook and Hodgkin 2007)mentioning

confidence: 99%

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Caenorhabditis elegans Mutants Resistant to Attachment of Yersinia Biofilms

et al. 2007

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Exploiting Genomics to Understand the Interactions Between Root-Knot Nematodes and Pasteuria penetrans

Schaff

Mauchline

Opperman

et al. 2011

Biological Control of Plant-Parasitic Nematodes:

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Caenorhabditis elegans was the first multicellular organism to have its genome sequenced and has proved useful in the investigations of innate immunity, the generic science that underpins the biology of host-pathogen interactions. This chapter explores the sequencing of plant-parasitic nematodes and microbial genomes and shows how this knowledge can help in understanding the biology of the interaction between Meloidogyne spp. and the bacterial nematode parasite Pasteuria penetrans. Three examples examine how genomic information can help in developing new approaches to the problems associated with using Pasteuria as a biological control agent: initially one focuses on the transportome and how genomics might help to understand the fastidious nature of Pasteuria growth in the nematode; secondly, comparative genomics is used to explore the phosphorylation pathway important in initiating sporulation; and, thirdly, comparative genomics is exploited to understand endospore attachment to the nematode cuticle where, in comparisons with other animal parasitic Bacillus spp., collagen-like fibres have been implicated. Finally the chapter suggests that genomics paves the way for the development of designer control agents but such an approach would not be without its critics.

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Cloning and sequence homology of a rat UDP-GalNAc:polypeptideN-acetylgalactosaminyltransferase

1995

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A UDP-GalNAc:polypeptide N-acetylgalactosaminyltransferase (polypeptide GalNAc transferase) cDNA was amplified from rat sublingual, submandibular and parotid glands, brain, skeletal muscle, and liver, using the polymerase chain reaction (PCR) and sequences derived from bovine polypeptide GalNAc transferase-Type 1 (polypeptide GalNAc transferase-T1). The transcripts encoding the rat sublingual gland and bovine enzymes were 91% identical in nucleotide sequence, except in their 5' and 3' untranslated regions. The enzymes encoded by the rat and bovine cDNAs were 559 amino acids in length and were virtually identical (98% amino acid sequence identity and 99.5% homologous overall). Northern blot analysis indicates that the polypeptide GalNAc transferase-T1 transcripts are expressed in many tissues but at widely differing levels. Although the amino acid sequence of polypeptide GalNAc transferase-T1 is conserved among mammals, the pattern of tissue expression varies between rats and humans. For example, the steady-state level of polypeptide GalNAc transferase-T1 transcript is quite low in lung relative to other rat tissues, whereas high expression of this transcript is detected in human lung. Therefore, we surmise that isoforms of polypeptide GalNAc transferase must exist and that isoforms are expressed in a tissue-dependent fashion. Searches of the GenBank database have revealed homologous sequences for several isoforms derived from several human tissues. In addition, hypothetical proteins from C. elegans also display strong homology; evidence suggests six ancestral isoforms of polypeptide GalNAc transferases may exist in C. elegans.

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Altered expression of an L1-specific, O-linked cuticle surface glycoprotein in mutants of the nematode Caenorhabditis elegans.

Cited by 28 publications

References 30 publications

Caenorhabditis elegans Mutants Resistant to Attachment of Yersinia Biofilms

Caenorhabditis elegans Mutants Resistant to Attachment of Yersinia Biofilms

Exploiting Genomics to Understand the Interactions Between Root-Knot Nematodes and Pasteuria penetrans

Cloning and sequence homology of a rat UDP-GalNAc:polypeptideN-acetylgalactosaminyltransferase

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