Musset-Bilal F et al. (1994) Worm Breeder's Gazette "Characterization of the C. elegans Basement Membrane-Associated Protein SPARC"

Musset-Bilal F, Schwarzbauer JE, Ryan CS

[Worm Breeder's Gazette, 1994]

Characterization of the C. elegans Basement Membrane- Associated Frederique Musset-Bilal, Carol S. Ryan, and Jean E. Schwarzbauer Department of Molecular Biology, Princeton University, Princeton NJ 08544

Abby F Dernburg et al. (2001) International C. elegans Meeting "Chromosome remodeling during meiosis"

Abby F Dernburg, Bobby Hogg, Carol Anderson

[International C. elegans Meeting, 2001]

This abstract is being submitted as a placeholder for a revised abstract to be entered during the week of April 20. This delay is necessary because we would like to include data from different lab personnel, and my rotation students (currently comprising the entire lab) will be making their final lab decisions that week. We are working on several questions regarding chromosome and chromatin remodeling. In particular, we are interested in how chromatin is remodeled during meiosis to accomplish chromosome pairing, crossing-over, and segregation.

Eve A (2021) Development "An interview with Swathi Arur."

Eve A

[Development, 2021]

Swathi Arur is an Associate Professor for the Department of Genetics at the MD Anderson Cancer Center, USA, where she uses multidisciplinary approaches to understand female germline development and fertility. She has received numerous accolades, including the MD Anderson Distinguished Research Faculty Mentor Award in 2017. In 2020, she was elected to the American Association for the Advancement of Science (AAAS). Swathi joined the team at Development as an Academic Editor in 2020, and we met with her over Zoom to hear more about her life, her career and her love for <i>C. elegans</i>.

Dixon JR (2019) Dev Cell "TADs for Life: Chromatin Domain Organization Regulates Lifespan in C.elegans."

Dixon JR

[Dev Cell, 2019]

In this issue of Developmental Cell, Anderson etal. (2019) show that chromatin domain structure on the X chromosome in C.elegans is dispensable for dosage compensation but regulates longevity and thermotolerance. This study sheds light on the mechanisms of domain formation in C.elegans and how these features affect physiology.

Antol, Weronika et al. (2022) MicroPubl Biol

Sychta, Karolina, Prokop, Zofia M., Antol, Weronika, Palka, Joanna K., Dudek, Katarzyna

[MicroPubl Biol, 2022]

Caenorhabditis elegans is a model species, increasingly used in experimental evolution studies to investigate such major topics as: maintenance of genetic variation, host-pathogen interaction and coevolution, mutations, life history, evolution of reproductive systems, sexual selection (Gray and Cutter, 2014; Teotnio, Estes, Phillips, and Baer, 2017). Its reproductive system in the wild, known as androdioecy, involves mostly self-fertilization of hermaphrodites and occasionally outcrossing with males, which are generally rare (Stewart and Phillips, 2002). This system can be experimentally changed to dioecy, i.e., obligatory outcrossing, through genetic manipulations (see Table I in Anderson, Morran, and Phillips, 2010; Gray and Cutter, 2014).

Kisiel MJ et al. (1969) Nematologica "Influence of a growth factor from bacteria on the morphology of C. briggsae."

Nelson B, Zuckerman BM, Kisiel MJ

[Nematologica, 1969]

Several investigators have reported that nutritional or environmental factors induce morphological variations in the "so-called' bacteriophagous nematodes. For example, Nigon & Dougherty described a morphological mutant of the free-living, self-fertilizing, hermaphroditic nematode Rhabditis (Caenorhabditis) briggsae that ensued following heat-treatment of progeny cultured on bacteria. Also Anderson reported that certain diagnostic features of an Acrobeloides sp., specifically the shape of the labial probolae and tail, varied significantly when the nematodes were grown on bacterial cultures as compared to those grown in soil. The current paper describes a consistent morphological variation in Caenorhabditis briggsae grown axenically on a meridic medium containing a growth factor from a bacterium as compared with nematodes reared on a growth factor from liver extract.

Anderson ARA et al. (1997) Fundamental and Applied Nematology "Nematode movement along a chemical gradient in a structurally heterogeneous environment. 2. Theory."

Young IM, Sleeman BD, Anderson ARA, Griffiths BS

[Fundamental and Applied Nematology, 1997]

The effects of structural heterogeneity on both chemical diffusion and nematode movement are examined with the development of a theoretical model. The model considers three factors affecting nematode movement: soil structure, nematode foraging strategy and chemotaxis. Using a continuous model, we develop a discrete system which allows nematode trails to be simulated in any of the four experimental conditions given by Anderson et al (1997). We show that structural heterogeneity causes mixed levels of attractant concentration over small areas as well as "fingering" of the attractant. Soil structural heterogeneity also restricts the foraging strategy of the nematode which then becomes a strategy to avoid structural "traps". The effect of localised increases in structural density is shown to increase significantly "fingering" of the attractant.

O'Connor SL et al. (1995) International C. elegans Meeting "smg-1, A GENE INVOLVED IN NONSENSE-MEDIATED mRNA DECAY."

O'Connor SL, Pulak RA, Anders KR, Anderson P

[International C. elegans Meeting, 1995]

The informational suppressor genes smg-1 through smg-7 play a role in identifying and degrading mRNAs that contain nonsense codons. In smg(+) genetic backgrounds, unc-54 nonsense and frameshift mutation-containing mRNAs are unstable. Mutations in any of the seven smg genes cause these mutant mRNAs to accumulate to near wild-type levels (see Pulak and Anderson. 1993. Genes and Dev. 7: 1885; Cali and Anderson, Abstract this meeting). We used three factor mapping and a microinjection assay to identify two overlapping cosmids, F56F2 and C14A12, that contain smg-1 (O'Connor, 1993 Meeting Abstract). Subsequent subcloning and microinjection experiments localized the smg-1 rescuing activity to a 10 kb region. Southern analysis of ten smg-1 alleles isolated in a mut-2(r459) background identifies insertions in three alleles (r904, r910, and r913). All three insertions map to the 10 kb rescuing region. A 4 kb subclone from the middle of the rescuing region identifies a single transcript of 7.8 kb on an N2 northern blot. The size of this transcript is altered in smg-1(r904) and smg-1(r913) mutants. Thus, it seems likely that this 7.8 kb transcript is smg-1. The large size of the putative smg-1 mRNA is consistent with the large size of the smg-1 mutational target. Partial cDNAs of this transcript have been identified and the isolation of full length clones is underway. Sequence analysis of genomic and cDNA clones predicts that SMG-1 protein contains a kinase domain. The C-terminal region of SMG-1 has approximately 50% identity over 400 AA to the kinase domain of several phosphatidylinositole 3-kinases. This homology appears to be limited to the kinase domain; no significant homologies to other regions of SMG-1 have been identified. Sequence analysis is continuing.

Hodgkin JA (1988) Worm Breeder's Gazette "informational suppression by male-abnormal mutations: new names, new data."

Hodgkin JA

[Worm Breeder's Gazette, 1988]

As previously reported (WBG 10-1: 112, 10-2: 30, etc.) mutations at six different loci act as allele-specific suppressors of mutations in a variety of genes: tra-2, unc-54, etc. These mutations also have characteristic morphological effects on the anatomy of the adult male tail and, to a lesser extent, of the hermaphrodite vulva. For this reason they have hitherto been assigned to the mab (male abnormal) gene category: mab-1, ed) and mab-12 through mab-16 (unpublished). However, they exhibit such a distinctive set of common properties that it has been decided (with the agreement of Andy Papp, Victor Ambros, Rock Pulak and Phil Anderson, who have been responsible for isolating most of these suppressor mutations) to assign them to a new gene

Pulak RA et al. (1989) Worm Breeder's Gazette "smg mutations affect accumulation of unc-54 nonsense and frameshift mRNAs."

Pulak RA, Anderson P

[Worm Breeder's Gazette, 1989]

Mutations in any of the six smg loci are allele-specific suppressors of a variety of mutations in unrelated genes (Papp et al., Pulak & Anderson, 1989 Meeting Abstracts). The smg-suppressible allele unc-54( r293) contains a small deletion of the unc-54 polyadenylation site. unc-54(r293) accumulates a small amount of an aberrantly large mRNA ( <10% wild-type levels). unc-54(r293); smg double mutants accumulate approximately wild-type amounts of the same large mRNA (Pulak & Anderson, 1989 Meeting Abstracts). We have tested whether smg mutations also affect accumulation of unc-54 mRNAs that contain frameshift or nonsense mutations. In many organisms, such translation terminating mutations accumulate reduced amounts of the corresponding mRNA. unc-54(e190) is a 401 base pair out-of-frame deletion in the central region of the gene (Dibb et al., 1985). unc-54 mRNA is barely detectable in e190 (at most a few percent of wild-type levels). unc- 54(e1300) is an amber mutation near the 3' end of the gene (Dibb et al. , 1985). e1300 accumulates a reduced but easily detected amount of unc-54 mRNA (approximately 20-30% of wild-type levels). smg mutations do not phenotypically suppress e190 or e1300, but they dramatically affect the amount of accumulated mRNA. Both unc-54(e190); smg and unc- 54(e1300); smg double mutants accumulate approximately wild-type amounts of unc-54 mRNA. Thus, function of the wild-type smg genes is required for instability of these mutant mRNAs. We are testing other sequenced mutations to determine whether smg mutations affect mRNA accumulation in all types of nonsense mutations, in all regions of the gene, and in all genes. (If they do, smg mutations might be valuable for identifying clones of genes for which amber alleles are available.)