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D L Riddle

Publications and source records attributed to D L Riddle.

At least 73 records · Page 4Linked to original sources
PubMed1988

Acidic intracellular pH shift during Caenorhabditis elegans larval development.

During recovery from the developmentally arrested, nonfeeding dauer stage of the nematode Caenorhabditis elegans, metabolic activation is accompanied by a decrease in intracellular pH (pHi). Phosphorus-31 nuclear magnetic resonance (31P NMR) analyses of perchloric acid extracts show that inorganic phosphate predominates in dauer larvae, whereas ATP and other high-energy metabolites are abundant within 6 hr after dauer larvae have been placed in food to initiate development. Although metabolic activation has been associated with an alkaline pHi shift in other organisms, in vivo 31P NMR analysis of recovering dauer larvae shows a pHi decrease from approximately 7.3 to approximately 6.3 within 3 hr after the animals encounter food. This shift occurs before feeding begins, and it coincides with, or soon follows, the developmental commitment to recover from the dauer stage, suggesting that control of pHi may be important in the regulation of larval development in nematodes.

Animals↗
PubMed1988

A Caenorhabditis elegans RNA polymerase II gene, ama-1 IV, and nearby essential genes.

The amanitin-binding subunit of RNA polymerase II in Caenorhabditis elegans is encoded by the ama-1 gene, located approximately 0.05 map unit to the right of dpy-13 IV. Using the amanitin-resistant ama-1(m118) strain as a parent, we have isolated amanitin-sensitive mutants that carry recessive-lethal ama-1 alleles. Of the six ethyl methanesulfonate-induced mutants examined, two are arrested late in embryogenesis. One of these is a large deficiency, mDf9, but the second may be a novel point mutation. The four other mutants are hypomorphs, and presumably produce altered RNA polymerase II enzymes with some residual function. Two of these mutants develop into sterile adults at 20 degrees but are arrested as larvae at 25 degrees, and two others are fertile at 20 degrees and sterile at 25 degrees. Temperature-shift experiments performed with the adult sterile mutant, ama-1(m118m238ts), have revealed a temperature-sensitive period that begins late in gonadogenesis and is centered around the initiation of egg-laying. Postembryonic development at 25 degrees is slowed by 30%. By contrast, the amanitin-resistant allele of ama-1 has very little effect on developmental rate or fertility. We have identified 15 essential genes in an interval of 4.5 map units surrounding ama-1, as well as four gamma-ray-induced deficiencies and two duplications that include the ama-1 gene. The larger duplication, mDp1, may include the entire left arm of chromosome IV, and it recombines with the normal homologue at a low frequency. The smallest deficiency, mDf10, complements all but three identified genes: let-278, dpy-13 and ama-1, which define an interval of only 0.1 map unit. The terminal phenotype of mDf10 homozygotes is developmental arrest during the first larval stage, suggesting that there is sufficient maternal RNA polymerase II to complete embryonic development.

Animals↗
PubMed1988

Lethal and amanitin-resistance mutations in the Caenorhabditis elegans ama-1 and ama-2 genes.

Mutants of Caenorhabditis elegans resistant to alpha-amanitin have been isolated at a frequency of about 1.6 x 10(-6) after EMS mutagenesis of the wild-type strain, N2. Four new dominant resistance mutations have been studied genetically. Three are alleles of a previously identified gene, ama-1 IV, encoding the largest subunit of RNA polymerase II. The fourth mutation defines a new gene, ama-2 V. Unlike the ama-1 alleles, the ama-2 mutation exhibits a recessive-lethal phenotype. Growth and reproduction of N2 was inhibited at a concentration of 10 micrograms/ml amanitin, whereas ama-2/+ animals were inhibited at 100 micrograms/ml, and 800 micrograms/ml was required to inhibit growth of ama-1/+ larvae. We have also determined that two reference strains used for genetic mapping, dpy-11(e224)V and sma-1(e30)V, are at least four-fold more sensitive to amanitin that the wild-type strain. Using an amanitin-resistant ama-1(m118) or ama-1(m322) strain as a parent, we have isolated amanitin-sensitive mutants that carry recessive-lethal ama-1 alleles. The frequency of EMS-induced lethal ama-1 mutations is approximately 1.7 x 10(-3), 1000-fold higher than the frequency of amanitin-resistance alleles. Nine of the lethal alleles are apparent null mutations, and they exhibit L1-lethal phenotypes at both 20 degrees and 25 degrees. Six alleles result in partial loss of RNA polymerase II function as determined by their sterile phenotypes at 20 degrees. All but one of these latter mutations exhibit a more severe phenotype at 25 degrees C. We have also selected seven EMS-induced revertants of three different ama-1 lethals. These revertants restore dominant resistance to amanitin. The selection for revertants also produced eight new dominant amanitin resistance alleles on the balancer chromosome, nT1.

Alleles↗
PubMed1988

Fine-structure genetics of ama-1, an essential gene encoding the amanitin-binding subunit of RNA polymerase II in Caenorhabditis elegans.

A fine-structure genetic map has been constructed for ama-1 IV, an essential gene in Caenorhabditis elegans encoding the amanitin-binding subunit of RNA polymerase II. Sixteen EMS-induced recessive-lethal mutations have been positioned in the gene by determining their intragenic recombination frequencies with m118, a mutation that confers dominant resistance to alpha-amanitin. The 16 mutants, all isolated in the ama-1(m118) background, include 13 that are early larval lethals, and three that are mid-larval lethals, at 25 degrees. Six of the mutants exhibit temperature-dependence in the severity of their phenotype. Intragenic recombination between the lethal site and the parental resistance mutation was detected by means of resistance to amanitin. Recombinants were detected at frequencies as low as 2 X 10(-6). The segregation of the closely linked flanking markers, unc-17 and unc-5, revealed whether the lethal mutation was to the left or the right of m118. By adding the distances between the extreme left and right mutations, the ama-1 gene is estimated to be 0.011 map unit long, with m118 positioned 0.004 map unit from the left-most lethal mutation. To order the lethal mutations with respect to each other, viable heteroallelic strains were constructed using the free duplication, mDp1[unc-17(e113) dpy-13(+) ama-1(+)]. The heteroallelic strains were sensitive to amanitin, and recombination events between the lethal mutations were specifically selected by means of the dominant amanitin resistance encoded on the recombinant chromosome. The segregation of outside markers revealed the left-right order of the lethal mutations. The position of mutations within the gene is nonrandom. Functional domains of the ama-1 gene indicated by the various lethal phenotypes are discussed.

Alleles↗
PubMed1988

Management of a patient with a diagnosis of bilateral plantar fasciitis and Achilles tendinitis. A case report.

This case report describes an approach for determining when fabricated orthoses might be useful in the treatment of a patient with foot-related problems. The patient is of special interest because she is an aerobics instructor, and her type of injury is relatively common. Particular emphasis in the report is placed on hypothesizing the cause of the patient's complaints and then basing treatment on that hypothesis.

Achilles Tendon↗
PubMed1988

Methods for taking subtalar joint measurements. A clinical report.

Physical therapists frequently evaluate the lower extremity, and this evaluation often includes measuring the subtalar joint neutral (STJN) position and subtalar joint (STJ) passive range of motion (PROM). This report critically reviews methods used to measure STJN position and STJ PROM. Standardized methods for taking these measurements, which have been clinically tested and appear to be theoretically sound, are presented. Although these methods are based on anatomical considerations, their reliability is less than optimal. However, these are the only methods of measuring STJN position and STJ PROM that have been tested adequately for reliability.

Biomechanical Phenomena↗
PubMed1987

Goniometric reliability in a clinical setting. Shoulder measurements.

The purpose of this study was to examine the intratester and intertester reliabilities for clinical goniometric measurements of shoulder passive range of motion (PROM) using two different sizes of universal goniometers. Patients were measured without controlling therapist goniometric placement technique or patient position during measurements. Repeated PROM measurements of shoulder flexion, extension, abduction, shoulder horizontal abduction, horizontal adduction, lateral (external) rotation, and medial (internal) rotation were taken of two groups of 50 subjects each. The intratester intraclass correlation coefficients (ICCs) for all motions ranged from .87 to .99. The ICCs for the intertester reliability of PROM measurements of horizontal abduction, horizontal adduction, extension, and medial rotation ranged from .26 to .55. The intertester ICCs for PROM measurements of flexion, abduction, and lateral rotation ranged from .84 to .90. Goniometric PROM measurements for the shoulder appear to be highly reliable when taken by the same physical therapist, regardless of the size of the goniometer used. The degree of intertester reliability for these measurements appears to be range-of-motion specific.

Adult↗
PubMed1985

A gene affecting production of the Caenorhabditis elegans dauer-inducing pheromone.

A nematode mutant lacking pheromone activity does not enter the developmentally arrested dispersal stage called the dauer larva unless exogenous pheromone is added to the growth medium, indicating that the pheromone is required for wild-type dauer larva formation. In contrast, a class of temperature-sensitive mutant forms dauer larvae even in the absence of detectable pheromone, indicating that such mutants bypass the normal pheromone requirement. A rapid bioassay of pheromone produced by individual nematodes has been developed for genetic analysis of pheromone production.

Animals↗
PubMed1985

Responses of the plant parasitic nematodes Rotylenchulus reniformis, Anguina agrostis and Meloidogyne javanica to chemical attractants.

Rotylenchulus reniformis, Anguina agrostis and Meloidogyne javanica respond differently to gradients of chemical attractants. In chemotaxis assays performed on agarose plates, R. reniformis L2 larvae oriented their movement to several common inorganic salts, cyclic AMP and AMP, as well as to germinated host plant seeds. M. javanica L2 larvae were attracted to germinated seeds, but not to the salts tested, and A. agrostis dauer larvae were not strongly attracted to any of 12 different tested agents, including host root or shoot tips. Attraction of R. reniformis to salts was measured by comparing different pairwise combinations of ions at equivalent concentrations. The indicated order of attractiveness was: Cl- greater than Na+ greater than C2H3O2- greater than Mg2+, NH4+, SO4(2-). The least attractive salts, (NH4)2 SO4 and MgSO4, were weakly attractive at an orientation threshold of 1 mM, whereas the most attractive salt, MgCl2, was strongly attractive at a threshold of 0.2 mM Cl-. 3',5' cyclic AMP was strongly attractive at a threshold of 0.05 mM, whereas 5'-AMP was a weak attractant. Some of these responses may affect the distribution of R. reniformis in its natural environment.

Adenosine Monophosphate↗
PubMed1985

Gene interactions affecting muscle organization in Caenorhabditis elegans.

Revertants of unc-15(e73)I, a paralyzed mutant with an altered muscle paramyosin, include six dominant and two recessive intragenic unc-15 revertants, two new alleles of the previously identified suppressor gene, sup-3 V, and a new suppressor designated sup-19(m210)V. The recessive intragenic unc-15 revertants exhibit novel alterations in paramyosin paracrystal structure and distribution, and these alterations are modified by interaction with unc-82(e1220)IV, another mutation that affects paramyosin. A strain containing both unc-15 and a mutation in sup-3 V that restores movement was mutagenized, and paralyzed mutants resembling unc-15 were isolated. Twenty mutations that interfere with suppression were divided into three classes (nonmuscle, sus-1, and mutations within sup-3) based on phenotype, genetic map position and dominance. The nonmuscle mutations include dumpy and uncoordinated types that have no obvious direct effect on muscle organization. Two recessive mutations define a new gene, sus-1 III. These mutations modify the unc-15(e73) phenotype to produce a severely paralyzed, dystrophic double mutant that is not suppressed by sup-3. Five semidominant, intragenic sup-3 antisuppressor mutations, one of which occurred spontaneously, restore the wild-type sup-3 phenotype of nonsuppression. However, reversion of these mutants generated no new suppressor alleles of sup-3, suggesting that the sup-3 antisuppressor alleles are not wild type but may be null alleles.

Animals↗
PubMed1984

Functional study of the Caenorhabditis elegans secretory-excretory system using laser microsurgery.

Individual cells of the Caenorhabditis elegans secretory-excretory system were ablated by laser microbeam in various larval stages. Effects on growth, molting, osmoregulation, fertility, longevity, and dauer larva formation were tested. Single-cell ablations did not prevent subsequent molting, but ablation of the pore cell or the duct cell resulted in the absence of the normal cuticular lining of the excretory duct following a molt. When the pore cell, duct cell, or excretory cell was ablated, the animals filled with fluid within 12-24 hr and died within a few days, producing very few progeny. Ablation of the excretory gland cell, on the other hand, had no obvious developmental or behavioral effects. Excretory activity was monitored in dauer larvae by observing pulsation of the excretory duct in conditions of differing osmolarity. The rate of pulsation was quite variable over time in conditions of low osmotic strength, but average five- to six-fold higher than that observed in buffered saline. These observations, combined with the effects of laser ablation, lead to the conclusion that one function of the excretory system is osmoregulation.

Caenorhabditis↗
PubMed1984

The Caenorhabditis elegans dauer larva: developmental effects of pheromone, food, and temperature.

Three environmental cues influence both the entry into and exit from the developmentally arrested dispersal stage called the dauer larva: a dauer-inducing pheromone, food, and temperature. The pheromone, which is a measure of population density, induces dauer larva formation at the second (L2) molt and inhibits recovery in a dose-dependent manner. Food acts competitively to reduce the frequency of dauer larva formation and to enhance recovery. The pheromone causes a specific extension of the second larval stage, coupled with a transient decrease in the growth rate of the L2. Second-stage larvae grown in the presence of added pheromone are morphologically distinguishable from L2 larvae grown without pheromone. We have named the pre-dauer L2 larva the L2d. Commitment to dauer larva formation can occur at the L2d molt. When L2d larvae are shifted out of pheromone to a lawn of E. coli just before the L2d molt, a few worms complete development into dauer larvae. In contrast, worms are essentially committed to the non-dauer life cycle by the first larval molt if the L1 larvae are not grown in appropriately high levels of pheromone. In the presence of pheromone, the percentage of dauer larva formation is enhanced at higher temperatures within the normal growth range. Temperature down-shifts induce dauer larva recovery. Temperature-shift experiments show that the enhancement of dauer larva formation requires exposure to the higher temperature around the L1 molt. Two sensory mutants defective in thermotaxis are altered in their sensitivity to the dauer-inducing pheromone, but their pheromone response retains temperature dependence. Response of dauer larvae to environmental cues is highly age dependent, with older dauer larvae exhibiting an increased tendency to recover.

Animals↗
PubMed1984

A pheromone-induced developmental switch in Caenorhabditis elegans: Temperature-sensitive mutants reveal a wild-type temperature-dependent process.

Formation of a developmentally arrested dispersal stage called the dauer larva is enhanced by a Caenorhabditis-specific pheromone and is inhibited by increasing amounts of food. Pheromone-induced dauer larva formation of three tested wild-type strains is temperature-dependent, so that an increased percentage of the population forms dauer larvae at 25 degrees C compared to lower temperatures. Dauer-defective mutants fail to respond to added pheromone, and some behavioral mutants affected in thermotaxis or egg-laying also exhibit abnormal responses. Temperature-sensitive (ts) dauer-constitutive mutants form dauer larvae at a restrictive temperature regardless of environmental stimuli. At the permissive temperature (17.5 degrees C), alleles of six out of seven dauer-constitutive genes tested overrespond to the dauer-inducing pheromone. All known mutations in daf-4 (eight alleles) and daf-7 (five alleles) produce a ts dauer-constitutive phenotype. One daf-4 and one daf-7 allele are suppressed by the amber nonsense suppressor, sup-7(st5). At least these two dauer-constitutive mutations are likely to cause production of nonfunctional rather than ts gene products. These mutations appear to indirectly result in a ts phenotype by enhancing the expression of a wild-type ts developmental process.

Animals↗
PubMed1983

RNA polymerase II from wild type and alpha-amanitin-resistant strains of Caenorhabditis elegans.

DNA-dependent RNA polymerases I, II, and III have been isolated from the soil nematode, Caenorhabditis elegans, and RNA polymerase II has been partially purified. The sensitivities of these enzymes to alpha-amanitin resemble those of the cognate enzymes from vertebrates. RNA polymerase II from C. elegans is 50% inhibited by 7 ng/ml of the amatoxin and RNA polymerase III by 80 micrograms/ml, whereas RNA polymerase I is insensitive to 500 micrograms/ml. We have obtained mutants of C. elegans which can grow and reproduce in concentrations of alpha-amanitin which arrest development of wild type animals. One of these mutants (DR432) has an altered RNA polymerase II which in partially purified extracts is 150 times less sensitive to the drug than the wild type enzyme. The mutation, ama-1(m130), in DR432 is dominant and maps near dpy-13 on linkage group IV. RNA polymerase II isolated from ama-1/+ heterozygotes contains equal proportions of two components, corresponding in alpha-amanitin sensitivity to the enzymes from DR432 and wild type. Thus, ama-1 appears to affect a subunit of RNA polymerase II.

Amanitins↗
PubMed1983

Developmental alterations in sensory neuroanatomy of the Caenorhabditis elegans dauer larva.

The anterior sensory ultrastructure of the C. elegans dauer larva was examined in several specimens and compared with that of the second-stage (L2) larva, which immediately precedes the dauer stage. In some instances comparisons were made with L3, postdauer L4, and adult stages. Whereas sensory structures in different nondauer stages closely resemble each other, including the inner labial sensilla, amphids, and deirids. The relative positions of the afferent tips of the two types of inner labial neurons are reversed in the dauer stage compared to the L2 and postdauer L4 stages. Inner labial neuron 1 rather than neuron 2 is more anterior in each of the six sensilla, and neuron 1 has an enlarged tip. The neuron 2 cilia are only one-third as long as those in the L2. Amphidial neurons c, d, g, and i and the amphidial sheath cell are altered in shape or position in the dauer stage. Neurons g and i are displaced posteriorly within the dauer amphidial channel. Neuron d has significantly more microvillar projections than do the d cells in L2, L3, or postdauer L4 larvae. Winglike processes of dauer neuron c form a 200 degrees-240 degrees arc in transverse section, including extensive overlap of the two cells. The arc in an L2 seldom spans more than 100 degrees, and overlap does not occur. While L2 larvae possess two separate bilateral amphidial sheath cells, the left and right sheath cells are often continuous in the dauer larva. Deirid sensory dendrites exhibit a dauer-specific structure and orientation. The tip of each neuron is attached to the body wall cuticle by a substructure not observed in L2 or postdauer L4 stages, and the neurons are oriented parallel to the longitudinal axis of the dauer larva. The deirid sensory terminals are oriented perpendicular to the cuticle in other stages. Reversible alterations in neural structure are discussed in the context of dauer-specific behavior.

Animals↗
PubMed1983

Fine structure of the Caenorhabditis elegans secretory-excretory system.

The secretory-excretory system of C. elegans, reconstructed from serial-section electron micrographs of larvae, is composed of four cells, the nuclei of which are located on the ventral side of the pharynx and adjacent intestine. (1) The pore cell encloses the terminal one-third of the excretory duct which leads to an excretory pore at the ventral midline. (2) The duct cell surrounds the excretory duct with a lamellar membrane from the origin of the duct at the excretory sinus to the pore cell boundary. (3) A large H-shaped excretory cell extends bilateral canals anteriorly and posteriorly nearly the entire length of the worm. The excretory sinus within the cell body joins the lumena of the canals with the origin of the duct. (4) A binucleate, A-shaped gland cell extends bilateral processes anteriorly from cell bodies located just behind the pharynx. These processes are fused at the anterior tip of the cell, where the cell enters the circumpharyngeal nerve ring. The processes are also joined at the anterior edge of the excretory cell body, where the excretory cell and gland are joined to the duct cell at the origin of the duct. Secretory granules may be concentrated in the gland near this secretory-excretory junction. Although the gland cells of all growing developmental stages stain positively with paraldehyde-fuchsin, the gland of the dauer larva stage (a developmentally arrested third-stage larva) does not stain, nor do glands of starved worms of other stages. Dauer larvae uniquely lack secretory granules, and the gland cytoplasm is displaced by a labyrinth of large, transparent spaces. Exit from the dauer stage results in the return of active secretory morphology in fourth-stage larvae.

Animals↗
PubMed1982

A pheromone influences larval development in the nematode Caenorhabditis elegans.

A Caenorhabditis-specific pheromone and the food supply influence both entry into and exit from a developmentally arrested juvenile stage called the dauer larva. The pheromone increases the frequency of dauer larva formation and inhibits recovery but does not affect adult behavior such as chemotaxis and egg laying. The fatty acid--like pheromone has been partially purified and characterized by a new bioassay. If similar developmental control mechanisms are used by parasitic nematodes, such mechanisms might be exploited to develop highly selective anthelmintic agents.

Animals↗