Li WQ et al. (1992) Worm Breeder's Gazette "Characterization of the Axonal Guidance and Outgrowth gene Unc-33"

Shaw JE, Li WQ, Herman RK

[Worm Breeder's Gazette, 1992]

Characterization of the axonal guidance and outgrowth gene unc-33 W. Li, R. K. Herman and J. E. Shaw Department of Genetics and Cell biology, University of Minnesota, St Paul, MN 55108

Howard RM et al. (2002) Genes Dev "C. elegans EOR-1/PLZF and EOR-2 positively regulate Ras and Wnt signaling and function redundantly with LIN-25 and the SUR-2 Mediator component."

Howard RM, Sundaram MV

[Genes Dev, 2002]

Due to a production error, the origin of the eor-1 and eor-2 gene names was printed without proper attribution. The eor genes have been independently identified by multiple groups, and eor stands for egl-1 suppressor (M. Hengartner, pers. comm.)/plasmid DiO uptake defective (M. Herman, pers. comm.)/raf enhancer (our work). We apologize for the oversight.

Zhou MH et al. (1996) Worm Breeder's Gazette "Liquid Culture of the Worms with a Fermentor"

Zhou MH, Yang H, Walthall WW

[Worm Breeder's Gazette, 1996]

The yield of C. elegans and their food (E.coli) are relatively low in the large liquid cultures growth (Koelle et al.,1994) and the whole growth process is tedious. Here we report the successful growth of C.elegans with a fermentor. The following protocol is based on the protocol by Michael Koelle and Tory Herman (1994) from Internet.

Herman RK (1996) Genetics "Worm spadework."

Herman RK

[Genetics, 1996]

I fell in love with Caenorhabditis elegans in the summer of '72. Our relationship was cemented four years later, 20 years ago now, by the publication of a paper in Genetics on C. elegans chromosome rearrangements (Herman et al. 1976). My pleasant assignment here is to describe the beginning of that work and to relate it to current worm cytogenetics and chromosome mechanics.

Toshia Myers et al. (2003) International Worm Meeting "What is the cellular focus of lin-35 Rb?"

Iva Greenwald, Toshia Myers

[International Worm Meeting, 2003]

Class A and class B synthetic Multivulva (synMuv) genes function in genetically redundant pathways to inhibit vulval fate specification. While the exact mechanism of inhibition in C. elegans is unknown, many synMuv genes encode proteins that have been implicated in transcriptional repression in other systems, such as the class B synMuv gene lin-35 Rb (Lu and Horvitz, 1998). The cellular focus of synMuv genes is currently unclear. Originally, synMuv genes were proposed to act non-autonomously to repress vulval fates from within the hyp7 (Herman and Hedgecock, 1990; Hedgecock and Herman, 1995), but were subsequently proposed to act autonomously within the vulval precursor cells (VPCs) (Lu and Horvitz, 1998; Thomas and Horvitz, 1999). It is also conceivable that synMuv genes, which in general are broadly expressed, may have more than one cellular focus. Determining the cellular focus of synMuv gene activity is critical to understanding their roles during vulval development and the signalling events that lead to the invariant pattern of VPC fates, as models for the role of synMuv genes depend on inferences about their cellular focus. For example, the existence of an inhibitory signal was inferred based on the interpretation that hyp7 is the focus of lin-15 (Herman and Hedgecock, 1990); additionally, the view that LIN-35 Rb and transcription factors activated by the Ras-MAP kinase cascade compete with target gene promoters to antagonize vulval induction (Lu and Horvitz, 1998) requires that the focus of lin-35 activity be the VPCs. Utilizing both mosaic analysis and tissue-specific promoters for rescue experiments, we are currently trying to determine the focus of class B synMuv gene lin-35. We will report on our progress at the meeting. Hedgecock E.M., and Herman R.K. (1995). Genetics 141, 989-1006; Herman R.K., and Hedgecock E.M. (1990). Nature 348, 169-171; Lu X., and Horvitz, H.R. (1998). Cell 95, 981-991; Thomas, J.H., and Horvitz, H.R. (1999). Development 126, 3449-3459.

TM Ratliff et al. (1999) International C. elegans Meeting "Identification of EGL-27 Molecular and Genetic Interactions"

TM Ratliff, MA Herman

[International C. elegans Meeting, 1999]

We are interested in the control of cell polarity during C. elegans development. Our approach has been to identify mutations which disrupt the polarity of the T cell in the hermaphrodite tail. Mutations in the Wnt gene lin-44 and in the frizzled- related gene lin-17 have been shown to cause a reversal and loss of T cell polarity, respectively (Herman et al., 1995; Sternberg and Horvitz, 1988). Mutations in egl-27 also cause a loss of T cell polarity as well as defects in QL daughter cell migration (Herman et al., 1999). These two processes are known to involve Wnt signals and pathways. In addition, certain egl-27 mutants and egl-27 RNAi animals display embryonic patterning defects. The amino terminus of the predicted egl-27 protein contains a region of similarity to MTA1 (Herman et al., 1999), a mammalian factor overexpressed in metastatic cells (Toh et al., 1994). Further analyses of the EGL-27 amino terminal sequence has revealed several regions of similarity to proteins involved in chromatin remodeling (Solari, F., Bateman, A. and Ahringer, J., pers. comm.). MTA1 has been shown to be a subunit of a novel complex displaying ATP-dependent chromatin-remodeling and histone deacetylase activities. Specifically, MTA1 appears to function as a transcriptional repressor (Xue et al., 1998). The carboxy terminus of EGL-27 is glutamine-rich, suggesting it may be involved in protein-protein interactions. We propose that EGL-27 is a bifunctional protein having both a transcriptional repression function and an as yet identified function. To better understand EGL-27 function we are determining those proteins which interact with EGL-27 at both the molecular and genetic levels. We are using the yeast two-hybrid system to screen for proteins that interact with either the amino terminal domain, carboxy terminal domain or full length EGL-27 protein. To identify genetic interactions, we are constructing and analyzing strains doubly mutant for a loss-of-function mutation in egl-27 and a mutation in specific genes involved in specifying cell polarity, Wnt signaling or chromatin remodeling.

Otsuka AJ (1990) Worm Breeder's Gazette "ALTERATIONS IN UNC-44 ALLELES"

Otsuka AJ

[Worm Breeder's Gazette, 1990]

Preliminary analysis of six spontaneous unc-44 alleles indicates that alterations occur over a fairly large region in the genomic DNA. Southern analysis of two alleles from E. Hedgecock (rh1013 and rf1042) and four alleles (mn259, mn339, q331, and st200) from R. Herman and other labs (kindly provided by C. Kari, R. Herman, W. Li, and J. Shaw) indicated that restriction fragment differences from wild type are associated with all six alleles (see Franco et al., C. elegans Meeting abstracts, 1989). The construction of preliminary restriction maps of unc-44 cosmid (B0350 and C44A, kindly provided by A. Coulson and J. Sulston) and phage (DD#LRF1 and DD#LRF6) clones allows the approximate positioning of mutant changes. The absolute orientations of the cosmid and phage clones are based on positioning of these clones on the cosmid map. The overlapping of the cosmid and phage clones has not yet been demonstrated. Unfortunately, the cosmid isolate that could quickly clarify the situation (C02C3) deleted during growth. [See Figure 1]

Hirabayashi J (1999) Trends in Glycosylation "Mutations in possible glycosylation genes, sqv-3, sqv-7 and sqv-8, of C. elegans cause abnormal vulval formation."

Hirabayashi J

[Trends in Glycosylation, 1999]

Apoptosis and gastrulation are critical biological events required for normal development of multicellular animals. As a glycobiologist, you may easily imagine that both of these phenomena involve specific carbohydrate recognition, but actually it is rather difficult to prove. The nematode C. elegans seems to be an ideal model animal for such a proof, because its complete cell lineages have already been established, and more recently, the genome project for this organism has been accomplished. In addition, vulval formation which consists of invagination of epitherial cells underlying the cuticular layer into the inner tissues has been well studied. Essentially, this process is analogous to gastrulation. Recently, 8 genes names sqv-1-8 have been identified as those involved in normal vulval formation by a representative C. elegans genetic group [Herman, T., Hartwieg, E., and Horvitz, R. (1999) Proc. Natl. Acad. Sci. USA, 96, 968-973]. To our surprise, it turned out that three of the (sqv-3,7,8) were quite similar to the known mammalian genes encoding glucuronyltransferase, galactose transferase, and sugar nucleotide transporter [Herman, T., and Horvitz, R. (1999) Proc. Natl. Acad. Sci. US 96, 974-979].

Riddle DL et al. (1980) Worm Breeder's Gazette "announcements"

Swanson MM, Riddle DL

[Worm Breeder's Gazette, 1980]

The Caehorhabditis Genetics Center (CGC), sponsored by the National Institute on Aging, was funded on September 30, 1979. Dr. Don Murray is the NIA Project Officer. As you know, the CGC is to be responsible for strain acquisition, banking and distribution. Strains will be available without cost to all qualified investigators pursuing genetics-related studies with C. elegans. Other CGC functions will include maintenance of the genetic map, coordination of genetic nomenclature and maintenance of a current data bank on all strains, including bibliographic information. During the first year, we will be developing a computerized system for storage and retrieval of this information. The program will be designed to allow other labs with CRT terminals remote access to the computer data files. We have recently mailed a questionnaire regarding your anticipated use of the Center's services. Since your responses may help us to modify the design of the services to be offered, we would appreciate your returning those questionnaires as soon as possible if you have not already done so. If you did not receive our mailing and anticipate using the CGC, please contact us. We plan to maintain a complete library of articles on Caenorhabditis, so we would appreciate it if you also would send us one copy of each of your Caenorhabditis publications. We have recently done a retrospective search of the literature and will soon be distributing a complete C. elegans bibliography as a supplement to this Newsletter. The new bibliography contains about 350 references, and we plan to update it with each future issue of the Newsletter. We would like to thank Bob Herman for the excellent job he has done as a volunteer stock distribution center. The immensely valuable work that Bob Herman and Bob Horvitz have done on the genetic map surely is apparent to everyone. Bob Herman will be supplying us with many strains he has received from other laboratories and we hope to have a relatively up-to-date C. elegans collection in a few months. The CGC is scheduled to be fully operational by the Fall of 1980, but some services are available now.

Alicia Melendez et al. (2001) International C. elegans Meeting "What is the cellular focus of SynMuv genes?"

Iva Greenwald, Alicia Melendez

[International C. elegans Meeting, 2001]

The synthetic Multivulva (synMuv) genes comprise two classes of genes, Class A and Class B, that act in the determination of vulval precursor cell (VPC) fates (Ferguson, E.L. and Horvitz, H.R.,1985,1989). A synthetic Multivulva phenotype is produced by two mutations, one in each of the two classes of genes. Mutations in one or more class A genes or one or more class B genes do not produce a Multivulva phenotype. It has been proposed that the class A and class B genes define two functionally redundant pathways that act to specify the non-vulval fate of the vulval precursor cells. We have previously shown that lin-13 behaves as a Class B SynMuv gene, a class that also includes genes encoding the tumor suppressor Rb and RbAp48, a protein that binds Rb. We have also shown that LIN-13 is a nuclear protein that contains multiple zinc fingers and a motif, LXCXE, that has been implicated in Rb binding. These results together suggested a role for LIN-13 in Rb-mediated repression of vulval fates. A Multivulva phenotype can in principle result from activation of a pathway or process that promotes vulval fates, or the inhibition of a pathway or process that represses vulval fates. Genes that influence this process can in principle act in an external signalling cell or in the VPCs. There have been two views to date. One view is that SynMuv genes act in an external signalling cell, hyp7, to control expression of a factor that antagonizes the effects of the inductive signal or otherwise to promote nonvulval fates (Herman and Hedgecock 1990). The other view is that SynMuv genes act in the VPCs to repress transcription of genes that are involved in vulval differentation (Lu and Horvitz 1998). The proposal that SynMuv genes act in hyp7 was based on genetic mosaic studies of a lin-15 mutation that concomitantly removes both Class A and Class B activities (Herman and Hedgecock 1990), and was supported by mosaic analysis of the Class B SynMuv gene lin-37 (Hedgecock and Herman 1995). Our findings that lin-13::lacZ and LIN-13::GFP are consistently expressed in hyp7 and are generally undetectable in VPCs at the time of VPC specification has been consistent with this view. If SynMuv genes act in hyp7 and not in the VPCs, they may promote the expression in hyp7 of an inhibitory factor that represses vulval fates. As it remains possible that some SynMuv genes act in hyp7 while others act in the VPCs, and as expression data can be misleading as to cellular focus, we have undertaken genetic mosaic analyses of various SynMuv genes. We will report on our progress and plans concerning mosaic analysis of lin-13 and lin-35 and expression of SynMuv genes in specific cells.