Colonnello A et al. (2020) Neurotox Res "Correction to: Comparing the Neuroprotective Effects of Caffeic Acid in Rat Cortical Slices and Caenorhabditis elegans: Involvement of Nrf2 and SKN-1 Signaling Pathways."

Tunez I, Rubio-Lopez LC, Aguilera-Portillo G, Silva-Palacios A, Evaristo-Priego Y, Santamaria A, Galvan-Arzate S, Cortez-Nunez S, Aschner M, Rangel-Lopez E, Chen P, Colonnello A, Robles-Banuelos B, Garcia-Contreras R

[Neurotox Res, 2020]

One of the authors has incorrect family name spelling in the original article_. Michael Ashner should read as Michael Aschner.

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.

Hengartner MO et al. (1992) Worm Breeder's Gazette "unc-50, a Gene Required for Acetylcholine Receptor Function, Encodes an Unfamiliar Protein"

Horvitz HR, Tsung N, Hengartner MO, Lewis JA

[Worm Breeder's Gazette, 1992]

unc-50, a gene requiired for acetylcholine receptor function, encodes an unfamiliar protein Michael Hengartner, Nancy Tsung, Jim Lewist, and Bob Horvitz HHMI, Dept. Biology, MIT, Cambridge, MA 02139, USA. t Division of Life Sciences, U. of Texas at San Antonio, San Antonio, IX 78249

Holway AH et al. (2007) J Cell Biol "Checkpoint silencing during the DNA damage response in Caenorhabditis elegans embryos"

Kim SH, Michael WM, La Volpe A, Holway AH

[J Cell Biol, 2007]

After publication of this manuscript, the authors noticed that two images (Fig. 4 B, top left and middle) had been duplicated from a previous publication (Holway, A.H., C. Hung, and W.M. Michael. 2005. Genetics. 169:14511460). Here we provide new images corresponding to these control experiments. The authors apologize for this oversight.

Michael Shapira et al. (2005) International Worm Meeting "Large scale transcriptional and functional analyses reveal central roles for a GATA transcription factor in Caenorhabditis elegans innate immune responses toward Pseudomonas aeruginosa infection."

Michal Ronen, Min Jiang, Stuart Kim, Jiming Rong, Brigham Hamlin, Michael Shapira, Man-Wah Tan, Marianne Campbell

[International Worm Meeting, 2005]

The opportunistic human pathogen Pseudomonas aeruginosa infects the worm Caenorhabditis elegans, when ingested, and causes its death within 3 days. We performed genome-wide gene expression analyses at early time points during P. aeruginosa infection, followed by a large scale RNAi-based functional analysis, to identify genes that respond to and protect from this infection. Transcriptional responses were distinct from general stress responses as previously described (e.g. Huffman et al., 2004), although some overlap exists, suggesting that the bulk of this response is a bona fide immune response and not a secondary effect of cellular damage or impaired metabolism. Induced genes included known as well as yet unknown, or putative, members of all levels of the innate immune system. Among the latter, genes encoding proteins with the yet uncharacterized DUF141 domain were noticeable in their importance for protecting worms from infection. We further unraveled the participation of the Sma/TGFbeta pathway and the intestinal GATA transcription factor, elt-2, in the regulation of the immune response. RT-PCR and functional analyses in RNAi treated worms showed that elt-2 is crucial for gene induction during infection, slowing pathogen accumulation in the intestine and improving survival. These results provide direct evidence for elt-2 being a pivotal nuclear regulator of immune responses in C. elegans. Additional evidence suggests that elt-2 may function downstream to the Sma/TGFbeta pathway.

Michael WM (2017) MicroPubl Biol "Asymmetric distribution of cyb-3 in 4-cell stage embryos."

Michael WM

[MicroPubl Biol, 2017]

Early embryos were fixed and stained with Mab F2F4 (green), shown to recognize CYB-3 (Michael, 2016), and DAPI, to illuminate the DNA (blue). Either wild type or par-4 mutant embryos were examined, after 24-hour incubation at 25C (the non-permissive temperature for the it47 allele of par-4). Anterior is to the left in all images. The data presented here reveals previously not shown data that depicts CYB-3 as asymmetrically distributed at the 4-cell stage. These data further support reported findings in Michael, 2016. There is more CYB-3 in the AB cell relative to its sister P1. In 4-cell embryos there is more CYB-3 in the EMS cell relative to its sister, P2. Thus, during P-lineage divisions, CYB-3 is asymmetrically distributed such that the somatic precursor receives more than its germline precursor sister cell. This asymmetry is abolished in par-4 mutant embryos, where all blastomeres contain equivalent amounts of CYB-3.

Michael Meyer et al. (2008) Development & Evolution Meeting "NUD-1 Functions in Germline Development and Localizes Asymmetrically During Spermatogenesis"

Jennifer Miskowski, Kim Caldwell, Michael Large, Michael Meyer, Guy Caldwell

[Development & Evolution Meeting, 2008]

The C. elegans NUD-1 protein is the structural and functional ortholog of the fungal NudC protein (1). NUD-1/NudC proteins are evolutionarily conserved and have been implicated in diverse processes such as asymmetrical cell division in yeast, nuclear migration in fungi, and neuronal migration in humans; however, their exact function is unknown. When NUD-1 levels are depleted in N2 hermaphrodites by RNAi, a variety of phenotypes are found, including sterility (1), indicating a role for NUD-1 in C. elegans gonad development. Observation of nud-1(RNAi) mutants revealed possible defects in both the germ line and somatic gonad. To distinguish between these, NUD-1 RNAi was performed in rrf-1 mutants, which are resistant to RNAi in the soma. The treated animals were sterile and exhibited a wide variety of defects, suggesting that NUD-1 functions in the germ line. NUD-1 knockdown in males also results in gonad defects; sperm are generated, but their viability cannot be tested by mating due to severe tail malformations. An antibody generated against a phosphorylated version of mammalian NUDC cross-reacts specifically in C. elegans and is being used in immunofluorescence studies. Robust staining was observed in the germ line of both hermaphrodites and males. Specifically, NUD-1 was found in perinuclear puncta in primary spermatocytes with more diffuse staining in secondary spermatocytes and spermatids. NUD-1 was found to colocalize with fibrous body membrane organelles (FBMOs) which are sperm-specific organelles derived from the Golgi. Like FBMOs, NUD-1 is asymmetrically segregated to developing spermatids and away from residual bodies. Recent data suggests that the asymmetrical localization of FBMOs and NUD-1 is generated by the same molecular mechanism.

Jing Liu et al. (2015) Conf Proc IEEE Eng Med Biol Soc "Image registration robust to sparse large errors."

Andrew CHISHOLM, Marian Chuang, Pamela Cosman, Jing Liu

[Conf Proc IEEE Eng Med Biol Soc, 2015]

Registration is difficult when images to be registered contain sparse but large-valued differences. We present a method for robust registration that ignores some fraction of large differences, while constraining the sparseness of these errors. We apply the method to stabilize microscopy videos of C. elegans tissues, in which bright moving filaments and tissue wounding appear as sparse large-valued differences. We demonstrate the advantage of the method on both synthetic and real data compared to state-of-the-art methods.

Shintoku Y et al. (2005) J Parasitol "Strongyloides ratti infection in the large intestine of wild rats, Rattus norvegicus."

Kimura E, Hasegawa H, Shintoku Y, Kondo S, Islam MZ, Kadosaka T, Itoh M

[J Parasitol, 2005]

The large intestine of a rat has been neglected almost completely as a site of Strongyloides sp. infection. We reported that adult Strongyloides ratti remained in the large intestine for more than 80 days, producing more number of infective larvae than small intestine adults, and therefore hypothesized that parasitism in this site could be a survival strategy. In wild rats, however, no study has focused on large intestine infections of Strongyloides. The present study revealed that 32.4% of 68 wild rats, Rattus norvegicus, had the infection of S. ratti in the large intestine, with an average of 4.7 worms. These worms harbored normal eggs in the uterus. In a laboratory experiment with S. ratti and Wister rats, daily output of infective larvae by 4.7 females in the large intestine was estimated to be 4,638.4, suggesting that a few parasites could play a role in the parasite transmission. Five species of nematode found in the wild rats showed seasonality in infection intensity, with highest intensities in March-May. The number of S. ratti in the large intestine was also highest in these months.

Watson A et al. (1993) Nature "The Caenorhabditis elegans genome sequencing project: first steps in automation."

Smaldon N, Watson A, Lucke R, Hawkins TL

[Nature, 1993]

Novel biochemical processes using magnetic particles have been automated to provide a robotic system to perform processes for large-scale shotgun sequencing.