Johnson, Christina K. et al. (2021) MicroPubl Biol

Miller III, David M., Johnson, Christina K., Bianchi, Laura

[MicroPubl Biol, 2021]

For Johnson, CK; Miller, DD; Bianchi, L (2021). Effect of the protease plasmin on C. elegans hyperactive DEG/ENaC channels MEC-4(d) and UNC-8(d). microPublication Biology. 10.17912/micropub.biology.000412.

Johnson TE (2005) J Gerontol A Biol Sci Med Sci "Genes, phenes, and dreams of immortality: the 2003 Kleemeier Award lecture."

Johnson TE

[J Gerontol A Biol Sci Med Sci, 2005]

The 2002 Kleemeier Award from the Gerontological Society of America was awarded to Thomas E. Johnson, PhD, of the University of Colorado at Boulder. Dr. Johnson was the pioneer who first applied genetic analyses to the study of the aging processes in Caenorhabditis elegans and who introduced the nematode as an aging model. Longer life span was chosen as a surrogate marker for slowed aging. Here Dr. Johnson describes his role(s) in the isolation of age-1, the first longevity mutant, which can more than double the life span and which slows the rate of aging more than twofold. He also reviews research suggesting conservation of function and applicability to intervention by pharmacological targeting of the Age-1 pathway. Current work by biotechnology companies targets this and other basic discoveries in an attempt to postpone human aging.

Denis Touroutine et al. (2006) Neuronal Development, Synaptic Function, and Behavior Meeting "A Genetic Screen for ACR-16-dependent Nicotinic Receptor Trafficking Mutants"

Joshua Johnson, Denis Touroutine, Janet Richmond, Anna Burdina

[Neuronal Development, Synaptic Function, and Behavior Meeting, 2006]

Individual C. elegans body wall muscles express two pharmacologically distinct nicotinic receptors: a levamisole-sensitive receptor and a levamisole-insensitive receptor. Recently we identified the alpha-7 like nicotinic receptor subunit ACR-16 as an essential component of the levamisole-insensitive receptor (Touroutine et.al. 2005). Several proteins regulating the trafficking and synaptic localization of the levamisole-sensitive receptor have been identified including UNC-50, UNC-74 and LEV-10. However, with the exception of RIC-3, which regulates the function of both body wall muscle nicotinic receptors, the molecular mechanisms specifically controlling ACR-16 receptor assembly, trafficking and localization are unknown. To identify molecules required for ACR-16 function, we have generated transgenic worms expressing an integrated ACR-16::GFP construct under the control of the muscle specific promoter of myo-3. This construct completely rescues the behavioral phenotype of unc-63(x37);acr-16(ok789) - worms in which both nicotinic receptor responses are absent, to that of the levamisole-resistant unc-63(x37) single mutant. Furthermore, the amplitude of the cholinergic current attributed to the ACR-16 receptor is fully restored in muscle patch clamp recordings, suggesting that the GFP tag does not significantly affect ACR-16 receptor function. Immunofluorescent staining with antibodies to the presynaptic cholinergic vesicular transporter protein UNC-17, confirmed that ACR-16::GFP is localized to post-synaptic sites. To validate our reagent as a reliable tool for a genetic screen, we explored the localization of ACR-16::GFP in ric-3 mutants: in these mutants ACR-16::GFP puncta are completely absent. We are now conducting a forward semi-clonal screen to identify mutants in which ACR-16::GFP is absent or mislocalized. In a pilot screen of 800 haploid genomes, we have identified several candidates in which ACR-16::GFP is mislocalized. We are currently SNP mapping these mutants.

Murakami S et al. (1996) West Coast Worm Meeting "LIFE-EXTENSION PATHWAY IN C.ELEGANS"

Johnson TE, Dames SA, Murakami S, Tedesco PM, Duhon SA

[West Coast Worm Meeting, 1996]

Life extension is conferred either by mutants extending adult life (Age), including age-1, daf-2, daf-23, daf-28, spe-26, and an allele of clk-1. Another mode of life extension is conferred by mutants delaying developmental stage (Clk), including clk-1, clk-2, clk-3, gro-1(Wong et al., 1995; Lakowski and Hekimi, 1996). Three groups have identified a life-extension pathway formed by some Daf mutations (Dorman et al., 1995; Larsen et al., 1995; Murakami and Johnson, 1996). We found that the pathway is not limited to Daf mutations but includes other types of the Age mutants (Murakami and Johnson, 1996). Interestingly, the pathway confers UV resistance, suggesting that UV resistance is a good indicator of Age. It is also consistent with the hypothesis that stress resistance is a rate limiting factor determining longevity. We are also testing whether the Age-pathway can confer other types of stress such as H2O2 and heat.

Hooper C (1991) The Journal of NIH Research "Old-aged mutant ninja nematodes' cool anti-age gene."

Hooper C

[The Journal of NIH Research, 1991]

Cowabugna, dudes! Those lean, gene-revealing machines have scored a most totally excellent victory in the battle to understand aging. We are, of course, talking about mutant ninja nematodes here. At a conference on aging in January at Cold Spring Harbor's Banbury Center, Thomas Johnson of the Institute for Behavioral Genetics at the University of Colorado in Boulder brought some dudes and dudettes from Capitol Hill up to date on the latest awesome achievements of the bodacious beasts know as Caenorhabditis elegans.

Cowden C et al. (1986) Worm Breeder's Gazette "a CCK-like neuropeptide in Ascaris."

Stretton AOW, Cowden C

[Worm Breeder's Gazette, 1986]

Our aim is to obtain peptides of known sequence from Ascaris in order to determine their mode of action using electrophysiological methods. Since McIntire and Horvitz (C. elegans CSH Abstracts 1985) showed that cholecystokinin-like immunoreactivity (CCK-LI) is present in certain neurons in C. elegans, we are initially investigating the role of a CCK-like peptide (CCK-LP) in the nervous system of Ascaris using anti-CCK8 antisera to detect and localize CCK-LI. Using the methods developed by Johnson (see Johnson and Stretton, Soc. Neurosci. Abstr. 9: 302; Sithigorngul, Johnson and Stretton, C. elegans CSH Abstracts 1985) we find that in Ascaris, CCK-LI is concentrated in 2 cells (AVF cells) in the ventral nerve cord, in 3 cells in the ventral ganglion, in 4 processes in the ventral cord, and in 2 processes in the lateral line. Thus the CCK-LP is concentrated in a small minority of the 180 neurons present in the anterior region of adult Ascaris.We have developed a procedure for extracting the CCK- LP from C. elegans and fractionating the extract on a C18 cartridge. High voltage paper electrophoresis shows that added radioiodinated CCK8 is chemically intact after this extraction and after fractionation. The CCK-LP was separated from more hydrophilic components with a 20-40% gradient of acetonitrile on reversed phase HPLC. RIA's detected CCK-LI associated with a peak of optical density. Addition of authentic CCK8 (non-sulfated) to the sample showed that the RIA-positive peak was close to, but distinctly separate from, CCK8. Assuming that the specific immunoreactivity of nematode CCK-LP and mammalian CCK8 is the same, we can obtain 100 pmoles from 60g of C. elegans. From this crude estimate, it seems that the levels of recoverable peptide are sufficient for amino acid sequence determination which is now our top priority.

Coleman-Hulbert, Anna L et al. MicroPubl Biol

Sedore, Christine A, Phillips, Patrick C, Coleman-Hulbert, Anna L, Driscoll, Monica, Banse, Stephan A, Lithgow, Gordon J, Guo, Max, Johnson, Erik

[MicroPubl Biol, 2019]

The authors, Coleman-Hulbert, AL; Johnson, E; Sedore, CA; Banse, SA; Guo, M2; Driscoll, M3; Lithgow, GJ; and Phillips, PC, submit the following correction. The first reference in the methods paragraph should be (Lucanic et al., 2017; Plummer et al., 2017) and should not be letteredaccordingly. We assayed lifespan in response to imatinib mesylate exposure in three Caenorhabditis species in triplicate using our previously published workflow (Lucanic et al. 2017a; b). should be corrected to: We assayed lifespan in response to imatinib mesylate exposure in three Caenorhabditis species in triplicate using our previously published workflow (Lucanic et al., 2017; Plummer et al., 2017).

Johnson TE (2013) Exp Gerontol "25 years after age-1: genes, interventions and the revolution in aging research."

Johnson TE

[Exp Gerontol, 2013]

This communication will briefly review more than 30 years of research on aging using the nematode Caenorhabditis elegans ("The Worm") as carried out in the labs of Tom Johnson. We will highlight research directions initiated in the 1980's, which were exciting for those of us trying to turn over a new leaf in aging research. In this narrative, I will discuss primarily the science that I and my lab have been involved with for the last 30 years. This area has been fascinating to those studying the sociology of science as modern aging research has moved to replace the simplistic, poorly controlled and outright fictitious approaches seen in much of the previous aging research.

Wang L et al. (2023) STAR Protoc "Protocols for treating C. elegans with pharmacological agents, osmoles, and salts for imaging and behavioral assays."

Wang L, Bianchi L, Graziano B

[STAR Protoc, 2023]

Research rigor can be enhanced by pairing genetic tools with pharmacology and manipulations of solutes or ions. Here, we present a protocol for treating C. elegans with pharmacological agents, osmoles, and salts. We describe steps for agar plate supplementation, addition of the compound to the polymerized plates, and using liquid culture for exposure to the chemical. Treatment type depends on the stability and solubility of each compound. This protocol is applicable to both behavioral and in vivo imaging experiments. For complete details on the use and execution of this protocol, please refer to Wang et al. (2022),¹ Fernandez-Abascal et al. (2022),² and Johnson et al. (2020).³.

Johnson TE et al. (1987) "Aging in C. elegans: Update 1986."

Foltz NL, Johnson TE

[1987]

Since the last review in this series [Johnson, 1985], many papers have appeared dealing directly with the aging process in both Caenorhabditis elegans and Turbatrix aceti. We will review this work and also briefly review other areas of C. elegans research that may impact on the study of aging. C. elegans has become a major biological model; four "News" articles in Science [Lewin, 1984a,b; Marx, 1984a,b] and inclusion as one of three developmental genetics models in a recent text [Wilkins, 1986] indicate its importance. Recent work has verified earlier results and has advanced progress toward new goals, such as routine molecular cloning. The aging studies reviewed here, together with new findings from other areas of C. elegans research, lay the groundwork for rapid advances in our understanding of aging in nematodes. Several areas of research in C. elegans have been reviewed recently: the genetic approach to understanding the cell lineage [Sternberg and Horvitz, 1984] and a brief summary of cell lineage mutants [Hedgecock, 1985]. The specification of neuronal development and neural connectivity has been a continuing theme in C. elegans research and reviews of these areas have also appeared [Chalfie, 1984; White, 1985]. A major genetic advance is the development of reliable, if not routine, mosaic analysis [Herman, 1984; Herman and Kari, 1985], which is useful for the genetic analysis of tissue-limited gene expression. Hodgkin [1985] reviews studies on a series of mutants involved in the specification of sex. These include her mutations that cause XO worms (normally males) to develop as hermaphrodites and tra mutations that change XX hermaphrodites into phenotypic males. The work on the structure and development of nematode muscle has been summarized by Waterston and Francis [1985]. A comprehensive review of aging research, containing useful reference material on potential biomarkers, has appeared [Johnson and Simpson, 1985], as well as a review including