[P244]: Isolation and characterization of a candidate component of UNC-6/netrin signaling in axon guidance and distal tip cell migration in C. elegans

Extremophilic microorganisms represent a unique source of novel natural products. Among them, cold adapted bacteria and particularly alpine microorganisms are still underexplored. Here, we describe the isolation and characterization of a novel Gram-positive, aerobic rod-shaped alpine bacterium (KRL4), isolated from sediments from the Karuola glacier in Tibet, China. Complete phenotypic analysis was performed revealing the great adaptability of the strain to a wide range of temperatures (5–40 °C), pHs (5.5–8.5), and salinities (0–15% w/v NaCl). Genome sequencing identified KRL4 as a member of the placeholder genus Exiguobacterium_A and annotation revealed that only half of the protein-encoding genes (1522 of 3079) could be assigned a putative function. An analysis of the secondary metabolite clusters revealed the presence of two uncharacterized phytoene synthase containing pathways and a novel siderophore pathway. Biological assays confirmed that the strain produces molecules with antioxidant and siderophore activities. Furthermore, intracellular extracts showed nematocidal activity towards C. elegans, suggesting that strain KRL4 is a source of anthelmintic compounds.

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Three C. elegans Rac proteins and several alternative Rac regulators control axon guidance, cell migration and apoptotic cell phagocytosis

Development ◽

10.1242/dev.128.22.4475 ◽

2001 ◽

Vol 128 (22) ◽

pp. 4475-4488 ◽

Cited By ~ 7

Author(s):

Erik A. Lundquist ◽

Peter W. Reddien ◽

Erika Hartwieg ◽

H. Robert Horvitz ◽

Cornelia I. Bargmann

Keyword(s):

Cell Migration ◽

Axon Guidance ◽

Apoptotic Cell ◽

Regulatory Proteins ◽

Axon Pathfinding ◽

C Elegans ◽

Cell Corpse ◽

And Function ◽

Redundant Functions ◽

Caenorhabditis Elegans Genome

The Caenorhabditis elegans genome contains three rac-like genes, ced-10, mig-2, and rac-2. We report that ced-10, mig-2 and rac-2 act redundantly in axon pathfinding: inactivating one gene had little effect, but inactivating two or more genes perturbed both axon outgrowth and guidance. mig-2 and ced-10 also have redundant functions in some cell migrations. By contrast, ced-10 is uniquely required for cell-corpse phagocytosis, and mig-2 and rac-2 have only subtle roles in this process. Rac activators are also used differentially. The UNC-73 Trio Rac GTP exchange factor affected all Rac pathways in axon pathfinding and cell migration but did not affect cell-corpse phagocytosis. CED-5 DOCK180, which acts with CED-10 Rac in cell-corpse phagocytosis, acted with MIG-2 but not CED-10 in axon pathfinding. Thus, distinct regulatory proteins modulate Rac activation and function in different developmental processes.

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The Nc1/Endostatin Domain of Caenorhabditis elegans Type Xviii Collagen Affects Cell Migration and Axon Guidance

The Journal of Cell Biology ◽

10.1083/jcb.152.6.1219 ◽

2001 ◽

Vol 152 (6) ◽

pp. 1219-1232 ◽

Cited By ~ 111

Author(s):

Brian D. Ackley ◽

Jennifer R. Crew ◽

Harri Elamaa ◽

Tania Pihlajaniemi ◽

Calvin J. Kuo ◽

...

Keyword(s):

Cell Migration ◽

Caenorhabditis Elegans ◽

Axon Guidance ◽

Ectopic Expression ◽

Basement Membranes ◽

Protein Isoforms ◽

Developmentally Regulated ◽

C Elegans ◽

Collagen Xviii ◽

Nc1 Domain

Type XVIII collagen is a homotrimeric basement membrane molecule of unknown function, whose COOH-terminal NC1 domain contains endostatin (ES), a potent antiangiogenic agent. The Caenorhabditis elegans collagen XVIII homologue, cle-1, encodes three developmentally regulated protein isoforms expressed predominantly in neurons. The CLE-1 protein is found in low amounts in all basement membranes but accumulates at high levels in the nervous system. Deletion of the cle-1 NC1 domain results in viable fertile animals that display multiple cell migration and axon guidance defects. Particular defects can be rescued by ectopic expression of the NC1 domain, which is shown to be capable of forming trimers. In contrast, expression of monomeric ES does not rescue but dominantly causes cell and axon migration defects that phenocopy the NC1 deletion, suggesting that ES inhibits the promigratory activity of the NC1 domain. These results indicate that the cle-1 NC1/ES domain regulates cell and axon migrations in C. elegans.

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