WormBook () is an open-access, online collection of original, peer-reviewed chapters on the biology of Caenorhabditis elegans and related nematodes. Since WormBook was launched in June 2005 with 12 chapters, it has grown to over 100 chapters, covering nearly every aspect of C.elegans research, from Cell Biology and Neurobiology to Evolution and Ecology. WormBook also serves as the text companion to WormBase, the C.elegans model organism database. Objects such as genes, proteins and cells are linked to the relevant pages in WormBase, providing easily accessible background information. Additionally, WormBook chapters contain links to other relevant topics in WormBook, and the in-text citations are linked to their abstracts in PubMed and full-text references, if available. Since WormBook is online, its chapters are able to contain movies and complex images that would not be possible in a print version. WormBook is designed to keep up with the rapid pace of discovery in the field of C.elegans research and continues to grow. WormBook represents a generic publishing infrastructure that is easily adaptable to other research communities to facilitate the dissemination of knowledge in the field.
WormBase (), a model organism database for Caenorhabditis elegans and other related nematodes, continues to evolve and expand. Over the past year WormBase has added new data on C.elegans, including data on classical genetics, cell biology and functional genomics; expanded the annotation of closely related nematodes with a new genome browser for Caenorhabditis remanei; and deployed new hardware for stronger performance. Several existing datasets including phenotype descriptions and RNAi experiments have seen a large increase in new content. New datasets such as the C.remanei draft assembly and annotations, the Vancouver Fosmid library and TEC-RED 5′ end sites are now available as well. Access to and searching WormBase has become more dependable and flexible via multiple mirror sites and indexing through Google.
The semidominant mutation Liguleless3-O (Lg3-O) causes a blade-to-sheath transformation at the midrib region of the maize (Zea mays L.) leaf. We isolated a full-length lg3 cDNA containing a knotted1-like family homeobox. Six Lg3-O partial revertant alleles caused by insertion of a Mutator (Mu) transposon and two deletion derivatives were isolated and used to verify that our knotted1-like cDNA corresponds to the LG3 message. In wild-type plants the LG3 mRNA is expressed in apical regions but is not expressed in leaves. In mutant plants harboring any of three dominant lg3 alleles (Lg3-O, -Mlg, and -347), LG3 mRNA is expressed in leaf sheath tissue, indicating that the Lg3 phenotype is due to ectopic expression of the gene. The Lg3-O revertant alleles represent two classes of Lg3 phenotypes that correlate well with the level of ectopic Lg3 expression. High levels of ectopic LG3 mRNA expression results in a severe Lg3 phenotype, whereas weak ectopic Lg3 expression results in a mild Lg3 phenotype. We propose that ectopic Lg3 expression early in leaf development causes the blade-to-sheath transformation, but the level of expression determines the extent of the transformation.Maize (Zea mays L.) leaf development is thought to be divided into three distinct stages (Sylvester et al., 1990(Sylvester et al., , 1996. In the first stage the vegetative meristem recruites an overlapping ring of founder cells that will form the next phytomer: a repeating segment of the maize plant composed of the leaf, internode, node, and bud (Galinat, 1959). In the second stage, a subset of the founder cells, the leaf founder cells divide equally into an undifferentiated primordium. During the third stage, growth and differentiation of the primordium occur to form the mature leaf. Maize leaves are divided into three parts: the sheath, the ligular region, and the blade, as shown in Figure 1. The proximal sheath wraps around the culm and provides support for the plant. The distal blade grows out from the main axis of the plant and is its major photosynthetic organ. The ligular region, composed of the ligule and two wedgeshaped auricles, separates the sheath from the blade. Many mutations affect maize leaf development and in particular disrupt or displace the blade-sheath boundary and the associated ligule and auricle (Freeling and Hake, 1985; Becraft et al., 1990; Becraft and Freeling, 1994; Fowler and Freeling, 1996; Harper and Freeling, 1996; Schichnes and Freeling, 1998).The semidominant Liguleless3-O (Lg3-O) mutation results in a blade-to-sheath transformation at the midrib region of the maize leaf (Fig. 1B; Fowler and Freeling, 1996). Blade, auricle, and ligule regions are replaced by sheath at the midrib region, and at the midrib the ligule is removed. The blade-to-sheath transformation in the Lg3-O mutant causes the ligule to develop at the new blade-sheath boundary, distal to the location of wild-type ligules. The displaced ligule gradually approaches the wild-type position at the leaf margin ( Fig. 1B; Muehlbauer et al., 1997). Homo...
Hox genes are highly conserved segmental identity genes well known for their complex expression patterns and divergent targets. Here we present an analysis of cis-regulatory elements in the Caenorhabditis elegans Hox gene egl-5, which is expressed in multiple tissues in the posterior region of the nematode. We have utilized phylogenetic footprinting to efficiently identify cis-regulatory elements and have characterized these with gfp reporters and tissue-specific rescue experiments. We have found that the complex expression pattern of egl-5 is the cumulative result of the activities of multiple tissue or local region-specific activator sequences that are conserved both in sequence and near-perfect order in the related nematode Caenorhabditis briggsae. Two conserved regulatory blocks analyzed in detail contain multiple sites for both positively and negatively acting factors. One of these regions may promote activation of egl-5 in certain cells via the Wnt pathway. Positively acting regions are repressed in inappropriate tissues by additional negative pathways acting at other sites within the promoter. Our analysis has allowed us to implicate several new regulatory factors significant to the control of egl-5 expression.
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