Gonzalez Rangel, Alan et al. (2021) International Worm Meeting "DAF-16/FoxO are necessary to induce Germ Cell apoptosis under starvation"

Navarro Gonzalez, Rosa E., Hubbard, Jane E, Gonzalez Rangel, Alan, Recillas-Targa, Felix

[International Worm Meeting, 2021]

1Departamento de Biología Celular y Desarrollo. Instituto de Fisiología Celular, UNAM, Circuito Exterior s/n, Ciudad Universitaria, Mexico D.F. 04510. 2Skirball Institute of Biomolecular Medicine, Departments of Cell Biology and Pathology, New York University School of Medicine, New York 10016. Correspondence: rnavarro@ifc.unam.mx Apoptosis is a conserved processe necesary to kept the homeostasis tissues, in the adult C. elegans germline nearly 50% of germ cells are eliminated by apoptosis in physiological conditions. Fuetheremore different kinds of stress such as heat shock or starvation increases germ cell apoptosis. LIN-35/Rb, the closest retinoblastoma homolog in the C. elegans genome, regulates germ cell apoptosis during normal and starvation conditions by downregulating ced-9/Bcl2 expression. Upon starvation, the expression of lin-35/Rb is up regulated at the gene and protein level. Our main goal is to understand how lin-35/Rb expression is regulated during starvation. We Use MODENCODE database to identified some transcription factors that probably bind to lin-35/Rb's putative promoter and we are testing if they might regulated its expression under stress. Among the transcription factors that we have found is DAF-16 the worm FoxO homolog. We found that DAF-16/FoxO is important to induce germ cell apoptosis upon fasting. By qPCR, we observed that daf-16/FoxO mutant animals show low levels of lin-35 expression under stress suggesting that this transcription factor might be important to regulate its expression under this condition. Using a transgene that expresses daf-16 specifically in the germline (mex-3::daf-16::gfp) in a daf-16 mutant background, we observed that daf-16 expression in the gonad is sufficient to induce germ cell apoptosis under starvation demonstrating that DAF-16 controls germ cell apoptosis in an autonomously manner. By immunoprecipitation, we would like to demonstrate that daf-16 binds lin-35 promoter. Our findings suggest an important role of DAF-16/FoxO in the gonad under stress by control the expression of LIN-35/Rb as key players of starvation-induced germ cell apoptosis.

Wong X et al. (2015) Dev Cell "Finding the Middlemen in Genome Organization."

Reddy KL, Wong X

[Dev Cell, 2015]

Chromatin domains associated with the nuclear lamina are generally heterochromatic and transcriptionally repressed. How they are recruited to and maintained at the nuclear periphery remains unclear. A recent study by Gonzalez-Sandoval et al. (2015) in Cell identifies a chromatin-binding protein that links repressive chromatin with the inner nuclear membrane.

Vrbanac A et al. (2017) Cell Host Microbe "An Elegan(t) Screen for Drug-Microbe Interactions."

Morton JT, Debelius JW, Knight R, Jiang L, Dorrestein P, Vrbanac A

[Cell Host Microbe, 2017]

Microbes affect drug responses, but mechanisms remain elusive. Two papers in Cell exploit C.elegans to infer anticancer drug mechanisms. Through high-throughput screens of drug-microbe-host interactions, Garcia-Gonzalez etal. (2017) and Scott etal. (2017) determine that bacterial metabolism underpins fluoropyrimidine cytotoxicity, providing a paradigm for unraveling bacterial mechanisms in drug metabolism.

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

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]

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.

Chalfie M (1998) Nature "Genome sequencing. The worm revealed."

Chalfie M

[Nature, 1998]

In 1983, John Sulston and Alan Coulson began to construct a complete physical map of the genome of the nematode worm Caenorhabditis elegans, and started what became known as the C. elegans Genome Project. At the time, several people wondered why John, who had just described all of the cell divisions in C. elegans (the cell lineage), was interested in this project rather than in a more 'biological' problem. He replied by joking that he had a "weakness for grandiose, meaningless projects". In 1989, as the physical map approached completion, the Genome Project, now including Bob Waterston and his group, embarked on the even more ambitious goal of obtaining the complete genomic sequence