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1.
K A Adames  J Gawne  C Wicky  F Müller  A M Rose 《Genetics》1998,150(3):1059-1066
In Caenorhabditis elegans, individuals heterozygous for a reciprocal translocation produce reduced numbers of viable progeny. The proposed explanation is that the segregational pattern generates aneuploid progeny. In this article, we have examined the genotype of arrested embryonic classes. Using appropriate primers in PCR amplifications, we identified one class of arrested embryo, which could be readily recognized by its distinctive spot phenotype. The corresponding aneuploid genotype was expected to be lacking the left portion of chromosome V, from the eT1 breakpoint to the left (unc-60) end. The phenotype of the homozygotes lacking this DNA was a stage 2 embryonic arrest with a dark spot coinciding with the location in wild-type embryos of birefringent gut granules. Unlike induced events, this deletion results from meiotic segregation patterns, eliminating complexity associated with unknown material that may have been added to the end of a broken chromosome. We have used the arrested embryos, lacking chromosome V left sequences, to map a telomere probe. Unique sequences adjacent to the telomeric repeats in the clone cTel3 were missing in the arrested spot embryo. The result was confirmed by examining aneuploid segregants from a second translocation, hT1(I;V). Thus, we concluded that the telomere represented by clone cTel3 maps to the left end of chromosome V. In this analysis, we have shown that reciprocal translocations can be used to generate segregational aneuploids. These aneuploids are deleted for terminal sequences at the noncrossover ends of the C. elegans autosomes.  相似文献   

2.
R E Rosenbluth  D L Baillie 《Genetics》1981,99(3-4):415-428
The Caenorhabditis elegans mutation e873, which results in a recessive uncoordinated phenotype (formerly named Unc-72) and which had been isolated after 32P treatment (Brenner 1974), has now been found to act as a crossover suppressor and to be associated with a translocation between linkage groups (LG's) III and V. The translocation has been named, eT1(III; V); eT1 acts as a dominant crossover suppressor for both the right half of LGIII and the left half of LGV, providing a balancer for a total of 39 map units. The uncoordinated e873 phenotype has been shown to be a consequence of an inactive unc-36III gene. It was possible to demonstrate that, in translocation heterozygotes, eT1 chromosomes marked with either sma-3 or dpy-11 segregate from normal LGIII, while those marked with bli-5, sma-2 or unc-42 segregate from normal LGV. Since bli-5 and sma-2 are normally on LGIII, and dpy-11 is normally on LGV, it is concluded that: (a) eT1 is a reciprocal translocation; (b) there is a breakpoint between sma-3 and sma-2 in LGIII (the region containing unc-36) and one between dpy-11 and unc-42 in LGV; (c) there is no dominant centromere between sma-2 and bli-5 on LGIII, since in eT1 these genes are not linked to a LGIII centromere. Similarly, it is highly unlikely that there is a centromere to the left of dpy-11 on LGV. The new gene order in eT1 was determined by measuring recombination rates between markers in eT1 homozygotes. It is concluded that the new order is: dpy-1 sma-3 (break) dpy-11 unc-60, and bli-5 sma-2 (break) unc-42 unc-51.--This is the first analysis of a C. elegans translocation with respect to reciprocity, breakpoints and new gene order.  相似文献   

3.
Link  Jana  Jantsch  Verena 《Chromosoma》2019,128(3):317-330

Vigorous chromosome movement during the extended prophase of the first meiotic division is conserved in most eukaryotes. The movement is crucial for the faithful segregation of homologous chromosomes into daughter cells, and thus for fertility. A prerequisite for meiotic chromosome movement is the stable and functional attachment of telomeres or chromosome ends to the nuclear envelope and their cytoplasmic coupling to the cytoskeletal forces responsible for generating movement. Important advances in understanding the components, mechanisms, and regulation of chromosome end attachment and movement have recently been made. This review focuses on insights gained from experiments into two major metazoan model organisms: the mouse, Mus musculus, and the nematode, Caenorhabditis elegans.

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4.
5.
We describe the distribution along the chromosomes of Caenorhabditis elegans of two repetitive DNA families, RcS5 and Cerep3 and interstitial telomeric sequences. Both families show, among other interesting features, a preferential location in the terminal 30% of the chromosomes. It is known that in these regions of the genome the frequency of recombination is much higher than in the central portion, genes are rarer and sequences important for chromosome disjunction may lie.  相似文献   

6.
The advantages of developing mutagenicity tests using the nematode, Caenorhabditis elegans, are discussed and an efficient in vivo test for detecting heritable autosomal recessive lethals over 40 map units is described. The test uses the reciprocal translocation, eTl(III;V), as a balancer. Dose-response curves for EMS (0.004–0.06 M) and γ-radiation (500–3000 R) were obtained. The spontaneous induction frequency for lethal mutations in 40 map units was found to be 0.06%. Mutations could be detected within 10 days and confirmed within another 5 days. From the point of view of C. elegans genetics, the EMS and γ-ray curves demonstrate that eTl can be used to test the efficacy of a particular mutagen in this organism. Although the present eTl protocol simultaneously screens hermaphrodite oocyte and sperm chromosomes, variations of the protocol that screen oocyte and sperm chromosomes separately are described.  相似文献   

7.
8.
The mammalian serum- and glucocorticoid-inducible kinase SGK1 regulates the endocytosis of ion channels. Here we report that in C. elegans sgk-1 null mutants, GFP-tagged MIG-14/Wntless, the sorting receptor of Wnt, failed to localize to the basolateral membrane of intestinal cells; instead, it was mis-sorted to lysosomes. This effect can be explained in part by altered sphingolipid levels, because reducing glucosylceramide biosynthesis restored the localization of MIG-14::GFP. Membrane traffic was not perturbed in general, as no obvious morphological defects were detected for early endosomes, the Golgi apparatus, and the endoplasmic reticulum (ER) in sgk-1 null animals. The recycling of MIG-14/Wntless through the Golgi might be partially responsible for the observed phenotype because the subcellular distribution of two plasma membrane cargoes that do not recycle through the trans-Golgi network (TGN) was affected to a lesser degree. Consistently, knockdown of the ArfGEF gbf-1 altered the distribution of SGK-1 at the basolateral membrane of intestinal cells. In addition, we found that sgk-1(RNAi) induced unfolded protein response in the ER, suggesting at least an indirect role of SGK-1 early in the secretory pathway. We propose that SGK-1 function is required for lipid homeostasis and that it acts at different intracellular trafficking steps.  相似文献   

9.
Neil A.  Croll  James M.  Smith 《Journal of Zoology》1978,184(4):507-517
Caenorhabditis elegans spends most of its life feeding. When feeding, it moves only short distances but intestinal contents are moved to and fro and thus mixed. The nematodes also defaecate and lay eggs during the feeding phase in bacterial culture. Defaecation is one of a series of events which causes the forward and backward movement of intestinal contents. These rhythmic movements, once initiated, appear to be controlled by a pacemaker and are unrelated to feeding rates. Oviposition is associated with movements of the genital tract and it can occur at any posture and does not influence the rate of other activities. After food-deprivation, C. elegans shows no measureable hunger response on being returned to bacteria. Experiments with excised parts of worms showed that isolated anterior ends will feed both in and out of bacteria and move forward and backward. Isolated posterior halves without a pharynx or circumpharyngeal commissure will lay eggs and defaecate.  相似文献   

10.
The sqt-1 gene is 1 of the several loci in Caenorhabditis elegans that primarily affects organismal morphology. Certain mutations in the sqt-1 gene can produce left roller animals, i.e., they rotate around their long axis and move in circular paths. We describe the morphological alterations seen in the cuticle of the left roller sqt-1(sc13). Deep-etched replica analyses showed that the fibrous layer is composed of a unique strand of parallel fibers, instead of the 2 meeting at an angle of 60 degrees as observed in the wild-type strain. In addition, honeycomb elements, fibers organized in a pentagonal fashion above the fibrous layer, completely fill the intermediate layer that is empty spaces in the wild type. These morphological alterations are likely to be involved in generating the helical twist of the sqt-1(sc13) left roller mutant.  相似文献   

11.
Annexins are structurally related proteins that bind phospholipids in a calcium-dependent manner. Recently, we showed that annexins IV, V, and VI also bind glycosaminoglycans in a calcium-dependent manner. Annexins are widely distributed from lower to higher eukaryotes, and the nematode Caenorhabditis elegans has been found to contain Nex-1, an annexin homologue. Here, we characterize the ligand-binding properties of Nex-1 using recombinant Nex-1. Nex-1 binds to liposomes containing phosphatidylserine. The apparent K(d) was calculated by Biacore to be 4.4 nM. Compared to mammalian annexins, the Nex-1 phospholipid-binding specificities were similar whereas the K(d) values were one order of magnitude larger. The Nex-1 glycosaminoglycan-binding specificities were investigated by affinity chromatography and solid-phase assays. Nex-1 binds to heparin, heparan sulfate, and chondroitin sulfate but not to chondroitin and chemically N- or O-desulfated heparin. Besides phospholipids, heparan sulfate and/or chondroitin (sulfate), probably on perlecan, could be endogenous ligands of Nex-1.  相似文献   

12.
Dystrobrevins are protein components of the dystrophin complex, whose disruption leads to Duchenne muscular dystrophy and related diseases. The Caenorhabditis elegans dystrobrevin gene (dyb-1) encodes a protein 38 % identical with its mammalian counterparts. The C. elegans dystrobrevin is expressed in muscles and neurons. We characterised C. elegans dyb-1 mutants and showed that: (1) their behavioural phenotype resembles that of dystrophin (dys-1) mutants; (2) the phenotype of dyb-1 dys-1 double mutants is not different from the single ones; (3) dyb-1 mutants are more sensitive than wild-type animals to reductions of acetylcholinesterase levels and have an increased response to acetylcholine; (4) dyb-1 mutations alone do not lead to muscle degeneration, but synergistically produce a progressive myopathy when combined with a mild MyoD/hlh-1 mutation. All together, these findings further substantiate the role of dystrobrevins in cholinergic transmission and as functional partners of dystrophin.  相似文献   

13.
A mutation in the gene gas-1 alters sensitivity to volatile anesthetics, fecundity, and life span in the nematode Caenorhabditis elegans. gas-1 encodes a close homologue of the 49-kDa iron protein subunit of Complex I of the mitochondrial electron transport chain from bovine heart. gas-1 is widely expressed in the nematode neuromuscular system and in a subcellular pattern consistent with that of a mitochondrial protein. Pharmacological studies indicate that gas-1 functions partially via presynaptic effects. In addition, a mutation in the gas-1 gene profoundly decreases Complex I-dependent metabolism in mitochondria as measured by rates of both oxidative phosphorylation and electron transport. An increase in Complex II-dependent metabolism also is seen in mitochondria from gas-1 animals. There is no apparent alteration in physical structure in mitochondria from gas-1 nematodes compared with those from wild type. These data indicate that gas-1 is the major 49-kDa protein of complex I and that the GAS-1 protein is critical to mitochondrial function in C. elegans. They also reveal the importance of mitochondrial function in determining not only aging and life span, but also anesthetic sensitivity, in this model organism.  相似文献   

14.
The site of the ribosomal gene cluster on embryonic metaphase chromosomes of Caenorhabditis elegans has been mapped by in situ hybridization using probe DNAs that have been nick-translated to incorporate biotin-labeled UTP. The hybridized probe DNA was detected by a double-layer fluorescent antibody technique. Since chromosomes from wild-type C. elegans embryos are indistinguishable, in situ hybridization was carried out with chromosomes from C. elegans strains carrying cytologically distinct translocation or duplication chromosomes in order to identify the right end of linkage group I as the site of the ribosomal genes. Chromosomes carrying a lethal mutation, let-209 I displayed smaller hybridization signals than wild-type, suggesting that these chromosomes carried a partial deficiency of the ribosomal gene cluster. A duplication of the ribosomal genes, eDp20(I;II) rescued let-209 homozygotes. Chromosomes carrying the alterations in the ribosomal genes were combined with mnT12(IV;X) to facilitate the mapping of genes in C. elegans by in situ hybridization. Linkage groups I and II are then labeled by the distinctive hybridization signals from the ribosomal probes, linkage groups IV and X are together distinguishable morphologically and linkage group V is labeled by hybridization to a 5S gene probe.  相似文献   

15.
The Caenorhabditis elegans genome contains a single dystrophin/utrophin orthologue, dys-1. Point mutations in this gene, dys-1(cx35) and dys-1(cx18), result in truncated proteins. Such mutants offer potentially valuable worm models of human Duchenne muscular dystrophy. We have used microarrays to examine genes expressed differentially between wild-type C. elegans and dys-1 mutants. We found 106 genes (115 probe sets) to be differentially expressed when the two mutants are compared to wild-type worms, 49 of which have been assigned to six functional categories. The main categories of regulated genes in C. elegans are genes encoding intracellular signalling, cell-cell communication, cell-surface, and extracellular matrix proteins; genes in these same categories have been shown by others to be differentially expressed in muscle biopsies of muscular dystrophy patients. The C. elegans model may serve as a convenient vehicle for future genetic and chemical screens to search for new drug targets.  相似文献   

16.
From analysis of ciné film, combined with ultrastructural observations, the anterior feeding structures and their behaviour in the free-living microbivorous nematode Caenorhabditis elegans during ingestion in dense and sparse suspensions of Escherichia coli are described In dense suspensions bacteria accumulate in the buccal cavity against the three metastomal flaps that nearly close it, and are then swallowed down the three tubular apical expansions of the triradiate oesophageal lumen when the flaps open. Excess medium is then expelled, as the oesophageal lumen closes and traps the swallowed bacteria. The flaps and oesophagus operate by contractions in the seven most anterior oesophageal muscle cells, probably coordinated via proprioceptive nerve endings between the cells. About one million nematode hours are needed to extract 1 g of bacteria from 30 ml of medium. With few or no bacteria, the head moves more, the metastomal flaps do not close and medium seems to pass in and out of the buccal cavity, probably as part of the widespread exploration phase of food-finding behaviour. Abnormal feeding behaviour, control and functions of the metastomal flaps and associated structures, and control of food intake volume are discussed.  相似文献   

17.
Xu X  Guo H  Wycuff DL  Lee M 《Experimental cell research》2007,313(11):2465-2475
During Caenorhabditis elegans ovulation, the somatic gonad integrates signals from germ cells and propels a mature oocyte into the spermatheca for fertilization. Previous work suggests that phosphoinositide signaling plays important roles in C. elegans fertility. To fully understand inositol-1,4,5-trisphosphate (IP(3)) signaling in ovulation, we have examined the function of phosphatidylinositol-4-phosphate 5' kinase (PIP5K) in C. elegans. Our results show that the C. elegans PIP5K homolog, ppk-1, is essential for ovulation in C. elegans; ppk-1 is mainly expressed in somatic gonad, and depletion of ppk-1 expression causes defective ovulation, reduced gonad sheath contractility, and sterility. Increased IP(3) signaling compensates for ppk-1 (RNAi)-induced sterility, suggesting that ppk-1 is linked to IP(3) signaling. These results demonstrate that ppk-1 plays an essential role in IP(3) signaling and cytoskeleton organization in somatic gonad.  相似文献   

18.
Type IV collagen is a major component of basement membranes. We have characterized 11 mutations in emb-9, the α1(IV) collagen gene of Caenorhabditis elegans, that result in a spectrum of phenotypes. Five are substitutions of glycines in the Gly-X-Y domain and cause semidominant, temperature-sensitive lethality at the twofold stage of embryogenesis. One is a glycine substitution that causes recessive, non–temperature-sensitive larval lethality. Three putative null alleles, two nonsense mutations and a deletion, all cause recessive, non–temperature-sensitive lethality at the threefold stage of embryogenesis. The less severe null phenotype indicates that glycine substitution containing mutant chains dominantly interfere with the function of other molecules. The emb-9 null mutants do not stain with anti–EMB-9 antisera and show intracellular accumulation of the α2(IV) chain, LET-2, indicating that LET-2 assembly and/or secretion requires EMB-9. Glycine substitutions in either EMB-9 or LET-2 cause intracellular accumulation of both chains. The degree of intracellular accumulation differs depending on the allele and temperature and correlates with the severity of the phenotype. Temperature sensitivity appears to result from reduced assembly/secretion of type IV collagen, not defective function in the basement membrane. Because the dominant interference of glycine substitution mutations is maximal when type IV collagen secretion is totally blocked, this interference appears to occur intracellularly, rather than in the basement membrane. We suggest that the nature of dominant interference caused by mutations in type IV collagen is different than that caused by mutations in fibrillar collagens.  相似文献   

19.
Oxidative stress, caused by free radicals within the body, has been associated with the process of aging and many human diseases. Because free radicals, in particular superoxide, are difficult to measure, an alternative indirect method for measuring oxidative stress levels has been used successfully in Escherichia coli and yeast. This method is based on a proposed connection between elevated superoxide levels and release of iron from solvent-exposed [4Fe-4S] enzyme clusters that eventually leads to an increase in hydroxyl radical production. In past studies using bacteria and yeast, a positive correlation was found between superoxide production or oxidative stress due to superoxide within the organism and electron paramagnetic resonance (EPR) detectable "free" iron levels. In the current study, we have developed a reliable and efficient method for measuring "free" iron levels in Caenorhabditis elegans using low-temperature Fe(III) EPR at g=4.3. This method uses synchronized worm cultures grown on plates that are homogenized and treated with desferrioxamine, an Fe(III) chelator, prior to packing the EPR tube. Homogenization was found not to alter "free" iron levels, whereas desferrioxamine treatment significantly raised these levels, indicating the presence of both Fe(II) and Fe(III) in the "free" iron pool. The correlation between free radical levels and the observed "free" iron levels was examined by using heat stress and paraquat treatment. The intensity of the Fe(III) EPR signal, and thus the concentration of the "free" iron pool, varied with the treatments that altered radical levels without changing the total iron levels. This study provides the groundwork needed to uncover the correlation among oxidative stress, "free" iron levels, and longevity in C. elegans.  相似文献   

20.
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