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[
Worm Breeder's Gazette,
1978]
All eyes are on the newest fashion trend, the Dumpy Look . Pace setting designer I.M. Worm s androgynous wardrobe is all the rage in Paris. Bianca Jagger quips, Tres, tres - Women s Wear Daily writes, Elegans personified - Patti Smith thinks, The punks won t buy it and Craig Russell says, It fits right in with my act . A product of Mutant Isolation, Inc.
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[
International Worm Meeting,
2013]
Self-avoidance, tiling and coexistence are the main mechanisms that enable the best dendritic coverage. C. elegans undergoes aging-associated changes that ultimately lead to decreased functionality of the organism, including its neurological functions. Recent research has shown that the nervous system of C. elegans undergoes changes and alterations during aging including dendritic morphology (Tank et al., 2011). We study dendritic plasticity, aging and spatial dendritic organization of two highly arborized mechanoreceptors in C. elegans, PVD and FLP (Oren-Suissa et al., 2010). PVD dendrites of L4s and young adults show regenerative ability following dendrotomy (laser induced severing of dendrites). Our working hypothesis is that in older ages this ability to regenerate is compromised. Previous studies and our preliminary results indicate that PVD and FLP do not overlap in larval stages (Smith et al., 2010). In addition, dendrites within each bilateral PVD do not overlap through a self-avoidance mechanism (Smith et al., 2012). We found that (1) the coverage fields of the PVD and FLP overlap in adult worms, which indicates coexistence and not tiling. This overlap increases as the worm ages. (2) PVDs show aberrant arborization at the age of 9 days of adulthood. (3) Dramatic increase in self-avoidance defects as animals age. In humans many neurodegenerative diseases as well as generalized cognitive decline are associated with age, aberrant arborization or both (e.g. autism and Alzheimer's disease). However our understanding of how these disorders are triggered and aggravated is scarce. Our research provides an insight into the aging and regeneration process of individual neurons. Oren-Suissa, M., et al. (2010). Science 328, 1285-1288. Smith, C.J. et al. (2010). Developmental Biology 345, 18-33. Smith, C.J., et al. (2012). Nature Neuroscience 15, 731-737. Tank, E.M.H. et al. (2011). Journal of Neuroscience 31, 9279-9288.
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[
J Cell Sci,
1983]
Studies of chromosome disposition at metaphase using serial thin-sectioning and three-dimensional reconstruction techniques have produced accurate estimates of the total volume of chromosomes per cell in 15 plant and two animal species. Comparing this character with the 4C DNA amount showed no indication of systematic differences in DNA density between either organisms with widely different (>200-fold) C values or different groups or organisms. For example, there was no significant difference between the density of DNA in somatic metaphase chromosomes of man (0.141 pg/um3) and its mean in 14 angiosperm plant species (0.182 pg/um3), or between four dicotyledons (0.180 pg/um3) and 10 monocotyledons (0.182 pg/um3). However, evidence was found showing that DNA density can vary significantly within a species. Thus, although the total chromosome volume per cell was closely correlated (r>0.97) with 4C DNA amount in somatic and meiotic cells, the density of DNA in metaphase chromosomes was significantly lower in meiocytes (0.131 pg/um3) than in somatic metaphase cells (0.179
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[
Worm Breeder's Gazette,
1980]
[See Figure 1] Already published allelism: Wood et al., 1980:
b117=
b189;
b246 = let- 2.Miwa et al., 1980:
hc57 =
hc62;
hc61 =
hc67. Our global complementation results:
g1 =
g4;
g16 =
g65 =
hc61 =
hc67;
g36 =
hc65;
g23 =
g34 =
hc70 =
b117 =
b189;
g37 =
b246 =
let-2;
b84 =
hc66;
g14 =
g43;
g57 =
b1O. From frequency of multiple alleles we estimate 200-400 genes essential for embryogenesis. Mapping is in progress. We are also doing tsp's, R + H Tests, and cellular defects ( Isnenghi, Cassada, Radnia, Schierenberg, K. Smith, v. Ehrenstein).
-
[
J Bacteriol,
2014]
Volume 195, no. 16, p. 35143523, 2013. A number of problems related to images published in this paper have been brought to our attention. Figure 1D contains duplicated images in lanes S and LE, and Fig. 4D and 6B contain images previously published in articles in this journal and in Microbiology and Microbial Pathogenesis, i.e., the following: C. G. Ramos, S. A. Sousa, A. M. Grilo, J. R. Feliciano, and J. H. Leitao, J. Bacteriol. 193:15151526, 2011. doi:10.1128/JB.01374-11. S. A. Sousa, C. G. Ramos, L. M. Moreira, and J. H. Leitao, Microbiology 156:896908, 2010. doi:10.1099/mic.0.035139-0. C. G. Ramos, S. A. Sousa, A. M. Grilo, L. Eberl, and J. H. Leitao, Microb. Pathog. 48:168177, 2010. doi: 10.1016/j.micpath.2010.02.006. Therefore, we retract the paper. We deeply regret this situation and apologize for any inconvenience to the editors and readers of Journal of Bacteriology, Microbial Pathogenesis, and Microbiology.
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[
International Worm Meeting,
2015]
In eukaryotes, multiple replication origins initiate DNA synthesis bidirectionally. Half of the genome is duplicated discontinuously on the lagging strand in the form of Okazaki Fragments (OFs). Previously we have purified and sequenced OFs from S. cerevisiae, and have demonstrated their utility in mapping genome wide DNA replication patterns (1,2). Despite many years of research, the precise location efficiency and abundance of replication origins in metazoa remains elusive. Here we capture and sequence OFs from C. elegans and generate a genome wide map of DNA replication.We use a DNA ligation compromised genetic background and purify single stranded OFs from developing embryos. Aligning sequence reads of OFs to the C. elegans genome reveals a characteristic strand bias at specific sites that are approximately 50-100 Kb apart. The complementary enrichment of Okazaki fragments to either the Watson or Crick strands is the hallmark of a replication origin. Additionally we have found that origins of replication in C. elegans are correlated with transcriptionally active regions of chromatin. Using the histone modification data set of modENCODE we found a strong association between replication start sites and acetylation of Histone H3 lysine 27 (H3K27ac). Acetylation of H3K27 is a chromatin mark characteristic of gene enhancer elements. Finally, we show that a partial depletion of CBP/P300 the sole histone H3 acetyltransferase (HAT) responsible for H3K27 acetylation has a profound effect on DNA replication. Our data indicate that the DNA replication program is likely plastic and is matched with the transcriptional program. Ultimately our data show, both DNA replication and gene transcription are likely regulated by similar epigenetic processes. 1. Intrinsic coupling of lagging-strand synthesis to chromatin assemblyDuncan J. Smith& Iestyn Whitehouse. Nature, 20122. Quantitative, genome-wide analysis of eukaryotic replication initiation and termination.McGuffee SR, Smith DJ, Whitehouse I. Mol Cell, 2013.
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[
J Theor Biol,
2019]
There are potential interactions between introns and their corresponding coding sequences (CDSs) in ribosomal protein genes that have been proposed by our group and the interactions are achieved by sequence matches between the two kinds of sequences. Here, the optimal matching relations between mature mRNAs and their corresponding introns in Caenorhabditis elegans (C.elegans) were investigated by improved Smith-Waterman local alignment software. Our results showed that the remarkably matched regions appear in the untranslated regions (UTRs) of mRNAs, especially in the 3' UTR. The optimal matched segments (OMSs) are highly organized segments. In addition, the optimal matching relations were analysed between mature mRNAs and other introns. The matching strengths in the UTRs are clearly lower than those in their corresponding introns. Our studies indicate that there are potential interactions between mature mRNAs and their corresponding introns and the post-spliced introns should have other novel functions in the gene expression process.
-
[
Am J Hum Genet,
2003]
Dyggve-Melchior-Clausen dysplasia (DMC) and Smith-McCort dysplasia (SMC) are similar, rare autosomal recessive osteochondrodysplasias. The radiographic features and cartilage histology in DMC and SMC are identical. However, patients with DMC exhibit significant developmental delay and mental retardation, the major features that distinguish the two conditions. Linkage studies localized the SMC and DMC disease genes to chromosome 18q12-21.1, providing evidence suggesting that they are allelic disorders. Sequence analysis of the coding exons of the FLJ90130 gene, a highly evolutionarily conserved gene within the recombination interval defined in the linkage study, identified mutations in SMC and DMC patients. The affected individuals in two consanguinous DMC families were homozygous for a stop codon mutation and a frameshift mutation, respectively, demonstrating that DMC represents the FLJ90130-null phenotype. The data confirm the hypothesis that SMC and DMC are allelic disorders and identify a gene necessary for normal skeletal development and brain function.
-
[
International C. elegans Meeting,
1997]
In C. elegans, a homologue of mammalian calreticulins was cloned and sequenced (M. Smith, DNA seq. 2: 235-40). This gene is composed of three exons and two introns and encodes a protein of 395 amino acid residues including an N-terminal signal sequence. The C-terminus contains an ER retention signal HDEL preceded by a polyacidic region similar to the mammalian calreticulins. Especially, the sequence displays 61% homology to mouse calreticulin, increasing up to 82% in the proline-rich region. This gene was designated as
crt-1 and mapped to the left end of chromosome V of the physical map. To observe the expression pattern of calreticulin in some tissues of C. elegans, we are currently constructing a genomic clone fused with GFP reporter, which will be injected into an animal to obtain transgenic lines. At the same time, a cDNA clone obtained by PCR will be used for over expression in E. coli to produce antibodies.
-
[
Genetics,
2018]
Modern experimental techniques, such as whole-genome sequencing and clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 endogenous genome editing, are enabling researchers to identify and further characterize the roles of proteins that were previously thought of as well defined. In the December 2016 issue of GENETICS, an article by Jaramillo-Lambert et al. identified a new role for the enzyme topoisomerase II in Caenorhabditis elegans male meiosis. This Primer article is designed to provide essential background information on C. elegans spermatogenesis and the relevant scientific techniques that will assist students and instructors in their understanding and discussion of the related article.Related article in GENETICS: Jaramillo-Lambert, A., A. S. Fabritius A. S., T. J. Hansen T. J., H. E. Smith H. E., and A. Golden A., 2016The identification of a novel mutant allele of topoisomerase II in Caenorhabditis elegans reveals a unique role in chromosome segregation during spermatogenesis. Genetics204: 1407-1422.