Hubbard EJA et al. (1994) Worm Breeder's Gazette "Genetic Analysis of sel-10."

Hubbard EJA, Greenwald IS

[Worm Breeder's Gazette, 1994]

Genetic analysis of sel-10 E. Jane Albert Hubbard and Iva Greenwald Department of Biochemistry and Molecular Biophysics and Howard Hughes Medical Institute, Columbia University, New York, New York, 10032

David Michaelson et al. (2006) Development & Evolution Meeting "Soma-germline Interactions Required for Robust Larval Germline Proliferation"

Rachael Lader, E. Jane Hubbard, David Michaelson, Dina Esposito, Chris Ryan, John Maciejowski, Jessica Dy-Johnson

[Development & Evolution Meeting, 2006]

Proper control of cell proliferation is critical for normal development. While the molecular basis for the proliferation/differentiation decision is relatively well-characterized in certain developmental contexts, less is known about cell-cell interactions that control of the extent of proliferation within a developing organ. The C. elegans germ line offers a tractable model system for exploring this problem. Previous work (McCarter et al., 1997; Killian and Hubbard, 2005), indicates that the distal pair of somatic gonadal sheath cells (Sh1) promote robust larval germline proliferation. We are taking several approaches to identify the molecular basis for this interaction. Forward genetic screens, molecular analysis and directed RNAi studies identified a critical role for optimal ribosome biogenesis in the sheath (Killian and Hubbard, 2004; Voutev et al., submitted) for its germline proliferation-promoting activity. To identify additional players, a genome-wide RNAi screen and candidate screens are underway. One screening strategy is based on the observation that reduced larval germline proliferation inhibits gonad arm extension, delays meiotic entry, and thereby uncouples the coordination between somatic gonad and germline development. As a result, under certain conditions, reducing larval germline proliferation can enhance proximal germline tumor formation (Pro phenotype; Killian and Hubbard, 2005; see also abstract by Maciejowski and Hubbard). Thus we are screening for soma-autonomous RNAi-induced enhancers of Pro. In addition, candidate screens suggest that the insulin pathway contributes to robust larval germline proliferation.

Chen X et al. (2015) Mol Neurodegener "Erratum to: Ethosuximide ameliorates neurodegenerative disease phenotypes by modulating DAF-16/FOXO target gene expression."

McCue HV, Chen X, Morgan A, Kashyap SS, Barclay JW, Kraemer BC, Burgoyne RD, Wong SQ

[Mol Neurodegener, 2015]

The original version of this article [1] unfortunately contained a mistake. The author list contained a spelling error for the author Hannah V. McCue. The original article has been corrected for this error. The corrected author list is given below:Xi Chen, Hannah V. McCue, Shi Quan Wong, Sudhanva S. Kashyap, Brian C. Kraemer, Jeff W. Barclay, Robert D. Burgoyne and Alan Morgan

Aric Rogers et al. (2007) International Worm Meeting "Post-transcriptional regulation downstream of the insulin-like signaling pathway in C. elegans."

Gordon Lithgow, Pankaj Kapahi, Di Chen, Aric Rogers, Gawain McColl, Alan Hubbard

[International Worm Meeting, 2007]

The insulin-like signaling (ILS) pathway plays a major role in the regulation of lifespan, metabolism, and neurodegenerative phenotypes in C. elegans. These phenotypes are modulated by gene expression downstream of the forkhead transcription factor DAF-16. A number of studies have used CHIP, SAGE, and microarrays to identify downstream mediators of DAF-16 at the genome-wide level. These studies have begun to resolve the complicated transcriptional network regulated by DAF-16 that determines certain phenotypes associated with ILS mutants. Additional elucidation may involve a better understanding of post-transcriptional regulation, as some studies in yeast and mammalian cells have reported a lack of correlation between the transcriptome and the proteome (Gygi et al. 1999, Ideker et al. 2001). Furthermore, deregulation of post-transcriptional processing and mRNA translation is now known as a crucial determinant in aging and age-related diseases including cancer, diabetes, and neurodegeneration. Despite intense study of ILS by numerous researchers, little is known about how DAF-16 and its direct as well as indirect targets affect post-transcriptional regulation of gene expression. We examined post-transcriptional changes in gene expression at the genome-wide level using a method referred to as translational state array analysis (TSAA). To measure the translation state of the mRNA, transcripts bound by ribosomes (polysomes) were separated using sucrose density gradient centrifugation. Resolved polysomes were fractionated according to low or high numbers of ribosomes bound per transcript. Unbound (untranslated) mRNA was also collected and all three fractions were analyzed using standard microarray techniques. We report that a number of genes previously shown to regulate lifespan and fat storage exhibit differences in post-transcriptional processing in a comparison of daf-2 and daf-2:daf-16 C. elegans mutants. Furthermore, the expression of numerous RNA-binding and mRNA translation regulating genes involved in post-transcriptional processing show changes in gene expression as assessed by mRNA ribosomal load. Preliminary lifespan analyses using RNAi-mediated gene suppression suggests that this method has been highly successful in identifying novel genes that determine lifespan in this pathway. Together, these results are the first to demonstrate vast post-transcriptional control by the ILS pathway in C. elegans. A better understanding of post-transcriptional processing within the ILS pathway will provide more insight into the basic mechanisms that determine longevity and metabolism.

Nariya, Hardik et al. (2017) International Worm Meeting "An investigation of the effects of artificial light at night on C. elegans offspring production and lifespan."

Buchanan, Bryant, Wise, Sharon, Zhushma, Rosa, Nariya, Hardik, Shinn-Thomas, Jessica

[International Worm Meeting, 2017]

Artificial light at night (ALAN) has many broad-scale and global implications for ecosystems and wildlife that have evolved under a 24-h circadian cycle. With increased urbanization, artificial light at night has directly altered natural photoperiods and nocturnal light intensity. Artificial light at night can disrupt behavioral patterns such as foraging activity and mating in animals. Disturbances in natural light and dark cycles also affect melatonin-regulated circadian and seasonal rhythms in Drosophila. We investigated the impact of ecologically relevant levels of light pollution on an important invertebrate model, Caenorhabditis elegans, as the impact of night lighting at these light levels is currently unknown. In this study, we exposed worms to artificial light at four intensities: 10-4 lx (control, comparable to natural nocturnal darkness), 10-2 lx (comparable to full-moon lighting and a low level of light pollution), 1 lx (comparable to dawn/dusk or intense light pollution), and 100 lx (dim daylight level comparable to extreme light pollution) on a 12L:12D photoperiod (100 lx treatments experienced constant light). We measured the impact of these light treatments on offspring production in hermaphroditic C. elegans. We grew worms for 2 generations in each light treatment, and then recorded the lifespan and counted the number of hatched offspring produced in the F3 generation. Our data show no significant differences among light levels for lifespan or offspring production suggesting that at least for these life history traits, ALAN does not affect these soil nematodes. Future directions include measuring additional life history traits and circadian gene expression for worms exposed to ALAN.

Coulson AR et al. (1989) Worm Breeder's Gazette "genome map."

Ameer H, Albertson DG, Sulston JE, Coulson AR, Waterston RH, Fishpool RM

[Worm Breeder's Gazette, 1989]

The map is now widely distributed electronically (see WBG 10(3), 67), but we are once again providing a summary for the gazette in the form of an output from the routine CHPLT. Do note that this is a provisional best guess, and that some linkages may later go away: please enquire if you need to know about the status of particular areas. When you receive cosmid clones, as stabs, please IMMEDIATELY streak them out on selective medium, pick small colonies, and grow 4ml minipreps (protocol from Alan Coulson if needed). For some cosmids, larger preps are liable to yield deleted DNA. Check that cosmid DNA appears full size (runs slower than lambda on agarose gels), then freeze a sample of good cells in 20% glycerol at -70 C. MRC computer account 'ARC' does not exist; Alan and John share account JES. A database node is now open at Seattle: modem number 206-467-2957; operator Phil Meneely. The summary of clone types given on the next page may be helpful when you are deciding which clones to request for your research. To reveal the most suitable clones for microinjection, the buried clones need to be displayed by the routine CONTASS; we will help you to do this if you ask. [See Figures 1- 3]

Diana Dalfo et al. (2008) Development & Evolution Meeting "RNAi screening to identify enhancers of the germline tumor phenotype in C. elegans"

E. Jane Hubbard, Diana Dalfo

[Development & Evolution Meeting, 2008]

There is significant interplay between the control of cell fate decisions and cell proliferation during development, yet the mechanisms underlying this interplay are not well understood. We are using the C. elegans germ line to investigate these mechanisms. C. elegans, germline polarity is established when a subset of previously undifferentiated germ cells differentiate and enter meiosis at a distinct developmental time and position. We have isolated mutants that disrupt the pattern of germline development such that the initial meiotic onset is delayed. The ultimate consequence of this delay is a large mass of proliferating germ cells in the proximal germ line of the adult. This phenotype, proximal proliferation (Pro), is observed with certain alleles of glp-1 (Pepper et al., 2003(a,b)). glp-1 is a receptor of the LIN-12/Notch family, and its activity promotes the proliferative or undifferentiated state and/or inhibits differentiation (meiosis) in the germ line (Austin and Kimble, 1987; Yochem and Greenwald, 1989). We are using a glp-1(Pro) allele as a starting point to identify additional factors that affect early germline proliferation and initial meiotic entry. Our previous data indicate that the distal pair of somatic gonadal sheath cells influence germline proliferation and act as an additional, non-DTC-mediated, mechanism to promote robust larval germline proliferation (Killian and Hubbard, 2005). We also observed that ablation of these cells enhances the glp-1(Pro) phenotype (Killian and Hubbard, 2005). Therefore, to identify the sheath-autonomous proliferation-promoting activity, we are performing candidate and genome-wide RNAi screens for enhancers of the Pro phenotype.

Scott AL (1996) Parasitol Today "Nematode sperm."

Scott AL

[Parasitol Today, 1996]

Parasitic nematode infections remain a major public health problem in many parts of the world. Because most of the current strategies aimed at controlling parasitic nematode infections have met with only limited success, it may be time to consider alternative approaches. An aspect of nematode biology that has drawn little attention as a target for control is the reproductive process. Although there are numerous facets of the overall reproductive biology of nematodes that hold potential as targets for intervention, Alan Scott here focuses on the male reproductive system, and outlines some of the known unique processes and characteristics of sperm formation and sperm function that could be exploited to block fertilization.

Consortium TCeGS (1995) Worm Breeder's Gazette "The C. elegans Genome Sequencing Project: A Progress Report."

Consortium TCeGS

[Worm Breeder's Gazette, 1995]

The C. elegans genome sequencing project: A progress report. The C. elegans Genome Consortium Genome Sequencing Center, Washington University School of Medicine, St. Louis, Missouri, USA and Sanger Centre, Hinxton Hall, Cambridge, UK. We present here another progress report for the C. elegans genome sequencing project. The majority of chromosome I*II is now essentially complete, although some gaps remain where cosmids were not available (Figure 1). While we are rescuing these regions from YACs and lambda clones, we will continue to sequence the cosmid-rich regions of other chromosomes. In the previous issue of the WBG, we reported significant protein similarities (blastx score >100) for several cosmids in the central region of chromosome II. Since then, we have made considerable progress on much of the remainder of this region. Protein similarities for several additional cosmids from chromosome II are presented in Table 1 (all cosmids for which shotgun sequencing has been completed). We also have begun sequencing cosmids near the center of the X chromosome. The St. Louis group started with cosmid C23F12 (near kin-11) and are moving right to left along the physical map. The Sanger Centre group are moving left to right from the same starting point. Similarity data for X chromosome cosmids which have been processed through the initial shotgun phase are also included in Table 1. For each putative genomic locus, the highest blastx score and a brief identifier are listed. Although the cosmids which contain database hits may not be completely sequenced, the Consortium will make preliminary sequence data available to the community with the caveat that it is preliminary and may still contain errors. Finished cosmid sequences are now available by anonymous ftp at: ftp.sanger.ac.uk (directory: pub/C.elegans_sequences). For further information on blastx similarities, please contact LaDeana Hillier (lhillier@watson.wustl.edu) or Steve Jones (sjj@sanger.ac.uk). For information on sequencing plans or estimated completion times, please contact Richard Wilson (rwilson@watson.wustl.edu) or Alan Coulson (alan@sanger.ac.uk). All requests for cosmid clones should be addressed to Alan Coulson. For further information about the C. elegans genome project including our policy statement about sharing both data and sequencing expertise, please contact Richard Wilson.

Greenwald IS (1984) Worm Breeder's Gazette "molecular cloning of lin-12."

Greenwald IS

[Worm Breeder's Gazette, 1984]

I have examined a total of eight independent lin-12 null mutations that arose spontaneously in a predominantly Bergerac genetic background. I probed genomic Southern blots with a 1.2 kb wild-type HindIII fragment that was defined by an insertion mutation (see last Newsletter) and/or with a cosmid 'contig' obtained from Alan Coulson and John Sulston that extends approximately 20 kb in each direction from the 1.2 kb HindIII fragment. The results thus far indicate that ( 1) seven of the eight mutations are associated with Tc1 insertions (2) the insertions are at different sites, and (3) all the insertion sites may lie within a single Pst fragment that is 2.8 kb in wild-type.