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Journal articles on the topic 'C. elegans'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 March 2025

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1

Sarkar, Ramin. "Treatment Analysis for Alzheimer’s Disease using Caenorhabditis Elegans as a Model." International Journal of Advanced Pharmaceutical Sciences and Research 4, no. 4 (June 30, 2024): 29–34. http://dx.doi.org/10.54105/ijapsr.a4057.04040624.

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Alzheimer's Disease, a progressive neurodegenerative condition lacking a definitive and guaranteed treatment, prompts critical investigation for effective remedies to manage its behavioral and cognitive impact. Herbal extracts like Ginkgo Biloba, Lion's Mane, Basil, and Sage present potential options to alleviate plaque build-up caused by Alzheimer's. This study aims to identify the most efficacious herbal extract for treating Alzheimer's, using aged Caenorhabditis elegans (C. elegans) as a model organism. The hypothesis states that treated C. elegans will exhibit increased behavioral movement and altered molecular effects compared to the untreated C. elegans. The Independent Variable consists of the various extracts fed to the C. elegans. The Dependent Variables consist of the C. elegan's behavioral abilities (speed, responsiveness, foraging) and C. elegan’s molecular effects measured by protein concentration. The Control Variable is the untreated aged C. elegan’s behavioral movement and molecular effects. Data was collected using WormLab and molecular assays to validate and determine the treatment's effectiveness. Through ANOVA testing, statistically significant differences emerged in four out of five measured tests, rejecting the null hypothesis more often than accepting it. Results from data indicate Ginkgo Biloba extract as the best extract, due to displaying increased speed, responsiveness, and foraging ability in C.elegans compared to other extracts and untreated C. elegans.This suggests Ginkgo Biloba as a highly possible treatment option.

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2

McKay, Renée M., James P. McKay, Leon Avery, and Jonathan M. Graff. "C. elegans." Developmental Cell 4, no. 1 (January 2003): 131–42. http://dx.doi.org/10.1016/s1534-5807(02)00411-2.

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3

Fodor, András. "Sydney Brenner ötven éve „mutatta be” a C. eleganst a genetikusoknak." Magyar Tudomány 186, no. 1 (January 24, 2025): 83–90. https://doi.org/10.1556/2065.186.2025.1.10.

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A Genetics folyóiratban ötven évvel ezelőtt (1974) jelent meg két későbbi Nobel-díjas (Sydney Brenner, Sir John Sulston) brit tudós ikerközleménye („A C. elegans genetikája”, „A C. elegans örökítőanyaga” címekkel), melynek tudománytörténeti jelentősége volt, amit az is bizonyít, hogy a C. eleganson dolgozó kutatók nyerték el a 2024-es fiziológiai és orvostudományi Nobel-díjat. Ez adta az alkalmat, hogy a Brenner- laboratóriumban a C. elegans hőskorában vendégkutatóként dolgozó magyar genetikus felidézze a kutatások lényegét és légkörét.

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4

SUGI, Takuma. "C. elegans Memory." Seibutsu Butsuri 52, no. 3 (2012): 144–45. http://dx.doi.org/10.2142/biophys.52.144.

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5

Chamberlin, Helen M. "C. elegans select." Nature Methods 7, no. 9 (September 2010): 693–95. http://dx.doi.org/10.1038/nmeth0910-693.

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6

Pettitt, Jonathan. "C. elegans II." Trends in Cell Biology 8, no. 2 (February 1998): 92. http://dx.doi.org/10.1016/s0962-8924(98)80022-6.

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7

Neff, Ellen. "C. elegans HeALTH." Lab Animal 49, no. 8 (July 23, 2020): 221. http://dx.doi.org/10.1038/s41684-020-0609-y.

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8

GENGYO, Keiko, Yasuhiro HATA, and Hiroaki KAGAWA. "Handling of C. elegans." Seibutsu Butsuri 27, no. 1 (1987): 42–45. http://dx.doi.org/10.2142/biophys.27.42.

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9

Starich, Todd, Melissa Sheehan, Joy Jadrich, and Jocelyn Shaw. "Innexins in C. elegans." Cell Communication & Adhesion 8, no. 4-6 (January 2001): 311–14. http://dx.doi.org/10.3109/15419060109080744.

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10

Weitzman, Jonathan B. "CDK7 in C. elegans." Genome Biology 3 (2002): spotlight—20020418–01. http://dx.doi.org/10.1186/gb-spotlight-20020418-01.

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11

Stoker, A. "C. elegans EPH receptor." Trends in Genetics 14, no. 5 (May 1998): 176. http://dx.doi.org/10.1016/s0168-9525(98)01491-7.

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12

Wood, William B. "Aging of C. elegans." Cell 95, no. 2 (October 1998): 147–50. http://dx.doi.org/10.1016/s0092-8674(00)81744-4.

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13

TISHECHKIN, DMITRI YU. "Review of the genus Taurotettix Haupt, 1929 (Homoptera: Cicadellidae: Deltocephalinae: Cicadulini): morphology, acoustic signals, and geographical variability." Zootaxa 5082, no. 2 (December 16, 2021): 191–99. http://dx.doi.org/10.11646/zootaxa.5082.2.9.

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The leafhopper genus Taurotettix includes two subgenera, Taurotettix (Taurotettix) and Taurotettix (Callistrophia), and three species, T. (T.) beckeri (Fieber, 1885), T. (C.) modesta (Mityaev, 1971), and T. (C.) elegans (Melichar, 1900). T. (C.) elegans is subdivided into two subspecies, T. (C.) elegans elegans and T. (C.) elegans subornata (Mityaev, 1971) stat. nov. Illustrated descriptions and data on biology and distribution for all taxa are given. Oscillograms of male calling signals of T. (T.) beckeri, T. (C.) modesta, and T. (C.) elegans elegans are provided. A hypothesis about speciation in Taurotettix (Callistrophia) is presented.

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14

Lu, Qun, Fan Wu, and Hong Zhang. "Aggrephagy: lessons from C. elegans." Biochemical Journal 452, no. 3 (May 31, 2013): 381–90. http://dx.doi.org/10.1042/bj20121721.

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Autophagy is a lysosome-mediated degradation process that involves the formation of an enclosed double-membrane autophagosome. Yeast genetic screens have laid the groundwork for a molecular understanding of autophagy. The process, however, exhibits fundamental differences between yeast and higher eukaryotes. Very little is known about essential autophagy components specific to higher eukaryotes. Recent studies have shown that a variety of protein aggregates are selectively removed by autophagy (a process termed aggrephagy) during Caenorhabditis elegans embryogenesis, establishing C. elegans as a multicellular genetic model to delineate the autophagic machinery. The genetic screens were carried out in C. elegans to identify essential autophagy genes. In addition to conserved and divergent homologues of yeast Atg proteins, several autophagy genes conserved in higher eukaryotes, but absent from yeast, were isolated. The genetic hierarchy of autophagy genes in the degradation of protein aggregates in C. elegans provides a framework for understanding the concerted action of autophagy genes in the aggrephagy pathway.

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15

VEIJOLA, Johanna, Pia ANNUNEN, Peppi KOIVUNEN, Antony P. PAGE, Taina PIHLAJANIEMI, and Kari I. KIVIRIKKO. "Baculovirus expression of two protein disulphide isomerase isoforms from Caenorhabditis elegans and characterization of prolyl 4-hydroxylases containing one of these polypeptides as their β subunit." Biochemical Journal 317, no. 3 (August 1, 1996): 721–29. http://dx.doi.org/10.1042/bj3170721.

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Protein disulphide isomerase (PDI; EC 5.3.4.1) is a multifunctional polypeptide that is identical to the β subunit of prolyl 4-hydroxylases. We report here on the cloning and expression of the Caenorhabditis elegans PDI/β polypeptide and its isoform. The overall amino acid sequence identity and similarity between the processed human and C. elegans PDI/β polypeptides are 61% and 85% respectively, and those between the C. elegans PDI/β polypeptide and the PDI isoform 46% and 73%. The isoform differs from the PDI/β and ERp60 polypeptides in that its N-terminal thioredoxin-like domain has an unusual catalytic site sequence -CVHC-. Expression studies in insect cells demonstrated that the C. elegans PDI/β polypeptide forms an active prolyl 4-hydroxylase α2β2 tetramer with the human α subunit and an αβ dimer with the C. elegans α subunit, whereas the C. elegans PDI isoform formed no prolyl 4-hydroxylase with either α subunit. Removal of the 32-residue C-terminal extension from the C. elegans α subunit totally eliminated αβ dimer formation. The C. elegans PDI/β polypeptide formed less prolyl 4-hydroxylase with both the human and C. elegans α subunits than did the human PDI/β polypeptide, being particularly ineffective with the C. elegans α subunit. Experiments with hybrid polypeptides in which the C-terminal regions had been exchanged between the human and C. elegans PDI/β polypeptides indicated that differences in the C-terminal region are one reason, but not the only one, for the differences in prolyl 4-hydroxylase formation between the human and C. elegans PDI/β polypeptides. The catalytic properties of the C. elegans prolyl 4-hydroxylase αβ dimer were very similar to those of the vertebrate type II prolyl 4-hydroxylase tetramer, including the Km for the hydroxylation of long polypeptide substrates.

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16

Berks, M. "The C. elegans genome sequencing project. C. elegans Genome Mapping and Sequencing Consortium." Genome Research 5, no. 2 (September 1, 1995): 99–104. http://dx.doi.org/10.1101/gr.5.2.99.

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17

Kitano, Hiroaki, Shugo Hamahashi, and Sean Luke. "The Perfect C. ELEGANS Project: An Initial Report." Artificial Life 4, no. 2 (April 1998): 141–56. http://dx.doi.org/10.1162/106454698568495.

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The soil nematode Caenorhabditis Elegans (C. elegans) is the most investigated of all multicellular organisms. Since the proposal to use it as a model organism, a series of research projects have been undertaken, investigating various aspects of this organism. As a result, the complete cell lineage, neural circuitry, and various genes and their functions have been identified. The complete C. elegans DNA sequencing and gene expression mapping for each cell at different times during embryogenesis will be identified in a few years. Given the abundance of collected data, we believe that the time is ripe to introduce synthetic models of C. elegans to further enhance our understanding of the underlying principles of its development and behavior. For this reason, we have started the Perfect C. elegans Project, which aims to produce ultimately a complete synthetic model of C. elegans' cellular structure and function. This article describes the goal, the approach, and the initial results of the project.

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18

Salinas, Gustavo, and Gastón Risi. "Caenorhabditis elegans: nature and nurture gift to nematode parasitologists." Parasitology 145, no. 8 (December 6, 2017): 979–87. http://dx.doi.org/10.1017/s0031182017002165.

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AbstractThe free-living nematode Caenorhabditis elegans is the simplest animal model organism to work with. Substantial knowledge and tools have accumulated over 50 years of C. elegans research. The use of C. elegans relating to parasitic nematodes from a basic biology standpoint or an applied perspective has increased in recent years. The wealth of information gained on the model organism, the use of the powerful approaches and technologies that have advanced C. elegans research to parasitic nematodes and the enormous success of the omics fields have contributed to bridge the divide between C. elegans and parasite nematode researchers. We review key fields, such as genomics, drug discovery and genetics, where C. elegans and nematode parasite research have convened. We advocate the use of C. elegans as a model to study helminth metabolism, a neglected area ready to advance. How emerging technologies being used in C. elegans can pave the way for parasitic nematode research is discussed.

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19

Tabuse, Y. "Protein Kinase C Isotypes in C. elegans." Journal of Biochemistry 132, no. 4 (October 1, 2002): 519–22. http://dx.doi.org/10.1093/oxfordjournals.jbchem.a003251.

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20

Chasnov, J. R., and King L. Chow. "Why Are There Males in the Hermaphroditic Species Caenorhabditis elegans?" Genetics 160, no. 3 (March 1, 2002): 983–94. http://dx.doi.org/10.1093/genetics/160.3.983.

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Abstract The free-living nematode worm Caenorhabditis elegans reproduces primarily as a self-fertilizing hermaphrodite, yet males are maintained in wild-type populations at low frequency. To determine the role of males in C. elegans, we develop a mathematical model for the genetic system of hermaphrodites that can either self-fertilize or be fertilized by males and we perform laboratory observations and experiments on both C. elegans and a related dioecious species C. remanei. We show that the mating efficiency of C. elegans is poor compared to a dioecious species and that C. elegans males are more attracted to C. remanei females than they are to their conspecific hermaphrodites. We postulate that a genetic mutation occurred during the evolution of C. elegans hermaphrodites, resulting in the loss of an attracting sex pheromone present in the ancestor of both C. elegans and C. remanei. Our findings suggest that males are maintained in C. elegans because of the particular genetic system inherited from its dioecious ancestor and because of nonadaptive spontaneous nondisjunction of sex chromosomes, which occurs during meiosis in the hermaphrodite. A theoretical argument shows that the low frequency of male mating observed in C. elegans can support male-specific genes against mutational degeneration. This results in the continuing presence of functional males in a 99.9% hermaphroditic species in which outcrossing is disadvantageous to hermaphrodites.

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21

Yu, Taoyuan, Xiping Xu, and Ning Zhang. "Network Flow Method Integrates Skeleton Information for Multiple C. elegans Tracking." Sensors 25, no. 3 (January 21, 2025): 603. https://doi.org/10.3390/s25030603.

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In order to solve the issues arising from collisions, this paper proposes a network flow method combined with skeleton information for multiple C. elegans tracking. In the intra-track stage, non-colliding C. elegans are identified and associated as trajectory fragments based on their motion and positional information, and colliding C. elegans are then segmented based on an improved skeleton algorithm and matched as trajectory fragments. Subsequently, the trajectory fragments are employed as vertices to construct a network flow model. The minimum-cost method is then utilized to solve the model, thereby obtaining the optimal solution for the multiple C. elegans trajectories. The proposed method was evaluated using video data of the C. elegans population at three distinct ages: L4, young adult, and D1. The experimental results demonstrate that the method proposed in this paper exhibits a MOTA between 0.86 and 0.92, and an MOTP between 0.78 and 0.83, which indicates that the proposed method can be employed in multiple C. elegans tracking. It is our hope that this method will prove beneficial to C. elegans laboratories, offering a novel approach to multiple C. elegans tracking.

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22

Bornhorst, Julia, Franziska Ebert, Sören Meyer, Vanessa Ziemann, Chan Xiong, Nikolaus Guttenberger, Andrea Raab, et al. "Toxicity of three types of arsenolipids: species-specific effects in Caenorhabditis elegans." Metallomics 12, no. 5 (2020): 794–98. http://dx.doi.org/10.1039/d0mt00039f.

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23

Holtzman, Eli J., Sumit Kumar, Carol A. Faaland, Fern Warner, Paul J. Logue, Sara J. Erickson, Gesa Ricken, Jeremy Waldman, Shiv Kumar, and Philip B. Dunham. "Cloning, characterization, and gene organization of K-Cl cotransporter from pig and human kidney and C. elegans." American Journal of Physiology-Renal Physiology 275, no. 4 (October 1, 1998): F550—F564. http://dx.doi.org/10.1152/ajprenal.1998.275.4.f550.

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We isolated and characterized the cDNAs for the human, pig, and Caenorhabditis elegansK-Cl cotransporters. The pig and human homologs are 94% identical and contain 1,085 and 1,086 amino acids, respectively. The deduced protein of the C. elegans K-Cl cotransporter clone (CE-KCC1) contains 1,003 amino acids. The mammalian K-Cl cotransporters share ∼45% similarity with CE-KCC1. Hydropathy analyses of the three clones indicate typical KCC topology patterns with 12 transmembrane segments, large extracellular loops between transmembrane domains 5 and 6 (unique to KCC), and large COOH-terminal domains. Human KCC1 is widely expressed among various tissues. This KCC1 gene spans 23 kb and is organized in 24 exons, whereas the CE-KCC1 gene spans 3.5 kb and contains 10 exons. Transiently and stably transfected human embryonic kidney cells (HEK-293) expressing the human, pig, and C. elegans K-Cl cotransporter fulfilled two (pig) or five (human and C. elegans) criteria for increased expression of the K-Cl cotransporter. The criteria employed were basal K-Cl cotransport; stimulation of cotransport by swelling, N-ethylmaleimide, staurosporine, and reduced cell Mg concentration; and secondary stimulation of Na-K-Cl cotransport.

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24

Hulbert, A. J. "Longevity, lipids and C. elegans." Aging 3, no. 2 (February 24, 2011): 81–82. http://dx.doi.org/10.18632/aging.100288.

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25

Hodgkin, J. "C. elegans: Sequence to Biology." Science 282, no. 5396 (December 11, 1998): 2011. http://dx.doi.org/10.1126/science.282.5396.2011.

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26

Silverman, P. H. "C. elegans as a Model." Science 284, no. 5412 (April 9, 1999): 261e—261. http://dx.doi.org/10.1126/science.284.5412.261e.

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27

Tang, Lin. "The C. elegans embryonic transcriptome." Nature Methods 16, no. 11 (October 31, 2019): 1079. http://dx.doi.org/10.1038/s41592-019-0643-0.

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28

Knight, K. "Ammonia excretion: C. elegans style." Journal of Experimental Biology 218, no. 5 (March 1, 2015): 647–48. http://dx.doi.org/10.1242/jeb.121012.

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29

Bettinger, J. C., and S. L. McIntire. "State-dependency in C. elegans." Genes, Brain and Behavior 3, no. 5 (October 2004): 266–72. http://dx.doi.org/10.1111/j.1601-183x.2004.00080.x.

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30

Hunt, Peter. "C. ELEGANS II (monograph 33)." Trends in Genetics 13, no. 10 (October 1997): 420. http://dx.doi.org/10.1016/s0168-9525(97)89752-1.

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31

Barr, Maureen M. "C. elegans male mating behavior." Seminars in Cell & Developmental Biology 33 (September 2014): 1–2. http://dx.doi.org/10.1016/j.semcdb.2014.06.006.

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32

Maduro, Morris F. "Gut development in C. elegans." Seminars in Cell & Developmental Biology 66 (June 2017): 3–11. http://dx.doi.org/10.1016/j.semcdb.2017.01.001.

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33

Chisholm, Andrew D., and Yishi Jin. "Neuronal differentiation in C. elegans." Current Opinion in Cell Biology 17, no. 6 (December 2005): 682–89. http://dx.doi.org/10.1016/j.ceb.2005.10.004.

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34

Suo, Satoshi, Shoichi Ishiura, and Hubert H. M. Van Tol. "Dopamine receptors in C. elegans." European Journal of Pharmacology 500, no. 1-3 (October 2004): 159–66. http://dx.doi.org/10.1016/j.ejphar.2004.07.021.

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35

Hammarlund, Marc, and Yishi Jin. "Axon regeneration in C. elegans." Current Opinion in Neurobiology 27 (August 2014): 199–207. http://dx.doi.org/10.1016/j.conb.2014.04.001.

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36

Ghosh, D. Dipon, Michael N. Nitabach, Yun Zhang, and Gareth Harris. "Multisensory integration in C. elegans." Current Opinion in Neurobiology 43 (April 2017): 110–18. http://dx.doi.org/10.1016/j.conb.2017.01.005.

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37

Palmisano, Nicholas J., and Alicia Meléndez. "Autophagy in C. elegans development." Developmental Biology 447, no. 1 (March 2019): 103–25. http://dx.doi.org/10.1016/j.ydbio.2018.04.009.

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38

Aamodt, Sandra. "Synaptic physiology in C. elegans." Nature Neuroscience 2, no. 9 (September 1999): 782. http://dx.doi.org/10.1038/12149.

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39

Alfred, Jane. "C. elegans — an innate choice?" Nature Reviews Genetics 3, no. 9 (September 2002): 651. http://dx.doi.org/10.1038/nrg893.

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40

Magnes, Jenny, Kathleen M. Raley-Susman, Alicia Jago, Karl Spuhler, Dylan Wine, and Tewa Kpulun. "Gravity Studies of C. elegans." Biophysical Journal 104, no. 2 (January 2013): 669a. http://dx.doi.org/10.1016/j.bpj.2012.11.3694.

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41

Keller, M. W., R. Mailler, and K. Adams. "Adhesion Energy of C. elegans." Experimental Mechanics 58, no. 8 (June 28, 2018): 1281–89. http://dx.doi.org/10.1007/s11340-018-0407-2.

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42

Alfred, Jane. "C. elegans — an innate choice?" Nature Reviews Immunology 2, no. 9 (September 2002): 632. http://dx.doi.org/10.1038/nri897.

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43

Le Bras, Alexandra. "Transcriptional adaptation in C. elegans." Lab Animal 49, no. 3 (February 25, 2020): 72. http://dx.doi.org/10.1038/s41684-020-0496-2.

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44

Emmons, Scott W. "Mechanisms of C. elegans development." Cell 51, no. 6 (December 1987): 881–83. http://dx.doi.org/10.1016/0092-8674(87)90574-5.

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45

Troemel, Emily R. "Chemosensory signaling in C. elegans." BioEssays 21, no. 12 (December 1, 1999): 1011–20. http://dx.doi.org/10.1002/(sici)1521-1878(199912)22:1<1011::aid-bies5>3.0.co;2-v.

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46

Ou, Chan-Yen, and Kang Shen. "Neuronal polarity in C. elegans." Developmental Neurobiology 71, no. 6 (May 6, 2011): 554–66. http://dx.doi.org/10.1002/dneu.20858.

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47

Zhu, Rain, and Ian D. Chin-Sang. "C. elegans insulin-like peptides." Molecular and Cellular Endocrinology 585 (May 2024): 112173. http://dx.doi.org/10.1016/j.mce.2024.112173.

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48

Pukkila-Worley, Read, Anton Y. Peleg, Emmanouil Tampakakis, and Eleftherios Mylonakis. "Candida albicans Hyphal Formation and Virulence Assessed Using a Caenorhabditis elegans Infection Model." Eukaryotic Cell 8, no. 11 (August 7, 2009): 1750–58. http://dx.doi.org/10.1128/ec.00163-09.

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ABSTRACT Candida albicans colonizes the human gastrointestinal tract and can cause life-threatening systemic infection in susceptible hosts. We study here C. albicans virulence determinants using the nematode Caenorhabditis elegans in a pathogenesis system that models candidiasis. The yeast form of C. albicans is ingested into the C. elegans digestive tract. In liquid media, the yeast cells then undergo morphological change to form hyphae, which results in aggressive tissue destruction and death of the nematode. Several lines of evidence demonstrate that hyphal formation is critical for C. albicans pathogenesis in C. elegans. First, two yeast species unable to form hyphae (Debaryomyces hansenii and Candida lusitaniae) were less virulent than C. albicans in the C. elegans assay. Second, three C. albicans mutant strains compromised in their ability to form hyphae (efg1Δ/efg1Δ, flo8Δ/flo8Δ, and cph1Δ/cph1Δ efg1Δ/efg1Δ) were dramatically attenuated for virulence. Third, the conditional tet-NRG1 strain, which enables the external manipulation of morphogenesis in vivo, was more virulent toward C. elegans when the assay was conducted under conditions that permit hyphal growth. Finally, we demonstrate the utility of the C. elegans assay in a screen for C. albicans virulence determinants, which identified several genes important for both hyphal formation in vivo and the killing of C. elegans, including the recently described CAS5 and ADA2 genes. These studies in a C. elegans-C. albicans infection model provide insights into the virulence mechanisms of an important human pathogen.

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49

Bornhorst, Julia, Eike Nustede, and Sebastian Fudickar. "Mass Surveilance of C. elegans—Smartphone-Based DIY Microscope and Machine-Learning-Based Approach for Worm Detection." Sensors 19, no. 6 (March 26, 2019): 1468. http://dx.doi.org/10.3390/s19061468.

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The nematode Caenorhabditis elegans (C. elegans) is often used as an alternative animal model due to several advantages such as morphological changes that can be seen directly under a microscope. Limitations of the model include the usage of expensive and cumbersome microscopes, and restrictions of the comprehensive use of C. elegans for toxicological trials. With the general applicability of the detection of C. elegans from microscope images via machine learning, as well as of smartphone-based microscopes, this article investigates the suitability of smartphone-based microscopy to detect C. elegans in a complete Petri dish. Thereby, the article introduces a smartphone-based microscope (including optics, lighting, and housing) for monitoring C. elegans and the corresponding classification via a trained Histogram of Oriented Gradients (HOG) feature-based Support Vector Machine for the automatic detection of C. elegans. Evaluation showed classification sensitivity of 0.90 and specificity of 0.85, and thereby confirms the general practicability of the chosen approach.

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50

Masler, Edward. "Comparison of alanine aminopeptidase activities in Heterodera glycines and Caenorhabditis elegans." Nematology 6, no. 2 (2004): 223–29. http://dx.doi.org/10.1163/1568541041218013.

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AbstractAminopeptidases in whole body homogenates of Caenorhabditis elegans and Heterodera glycines were detected using a colorimetric assay with a series of seven aminoacyl p-nitroanilide substrates. Enzyme properties evaluated included substrate preference and stability in response to metal salts, alcohols and storage. The preferred substrate for both species was Ala-pNA, but C. elegans had a much broader substrate range than H. glycines. All substrates were more active in C. elegans than in H. glycines homogenates, except Pro-pNA which was three times more active than in H. glycines. Ca 2+, Mg 2+ and Zn 2+ inhibited C. elegans activity in a dose responsive manner but had little effect on H. glycines aminopeptidase, and Co 2+ was mildly inhibitory in both species. Ethanol inhibited both C. elegans and H. glycines aminopeptidases but methanol inhibited only H. glycines and increased C. elegans activity. Heterodera glycines aminopeptidase was more stable at room temperature than C. elegans.

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