scholarly journals A Caenorhabditis elegans RNA-Directed RNA Polymerase in Sperm Development and Endogenous RNA Interference

Genetics ◽  
2009 ◽  
Vol 183 (4) ◽  
pp. 1297-1314 ◽  
Author(s):  
Jonathan I. Gent ◽  
Mara Schvarzstein ◽  
Anne M. Villeneuve ◽  
Sam Guoping Gu ◽  
Verena Jantsch ◽  
...  
Keyword(s):  
Rna Interference ◽  
Caenorhabditis Elegans ◽  
Rna Polymerase ◽  
Sperm Development

scholarly journals Multiple Subunits of the Caenorhabditis elegans Anaphase-Promoting Complex Are Required for Chromosome Segregation During Meiosis I

Genetics ◽  
2002 ◽  
Vol 160 (2) ◽  
pp. 805-813 ◽  
Author(s):  
Edward S Davis ◽  
Lucia Wille ◽  
Barry A Chestnut ◽  
Penny L Sadler ◽  
Diane C Shakes ◽  
...  
Keyword(s):  
Rna Interference ◽  
Caenorhabditis Elegans ◽  
Chromosome Segregation ◽  
Sister Chromatid ◽  
Sister Chromatid Cohesion ◽  
Anaphase Promoting Complex ◽  
Genetic Screens ◽  
Chromatid Cohesion ◽  
Interference Studies ◽  
Meiosis I

Abstract Two genes, originally identified in genetic screens for Caenorhabditis elegans mutants that arrest in metaphase of meiosis I, prove to encode subunits of the anaphase-promoting complex or cyclosome (APC/C). RNA interference studies reveal that these and other APC/C subunits are essential for the segregation of chromosomal homologs during meiosis I. Further, chromosome segregation during meiosis I requires APC/C functions in addition to the release of sister chromatid cohesion.

scholarly journals The nucleoporin Nup205/NPP-3 is lost near centrosomes at mitotic onset and can modulate the timing of this process in Caenorhabditis elegans embryos

2012 ◽  
Vol 23 (16) ◽  
pp. 3111-3121 ◽  
Author(s):  
Virginie Hachet ◽  
Coralie Busso ◽  
Mika Toya ◽  
Asako Sugimoto ◽  
Peter Askjaer ◽  
...  
Keyword(s):  
Cell Division ◽  
Rna Interference ◽  
Caenorhabditis Elegans ◽  
Nuclear Envelope ◽  
Aurora A Kinase ◽  
Aurora A ◽  
Time And Space ◽  
Local Loss ◽  
Necessary And Sufficient

Regulation of mitosis in time and space is critical for proper cell division. We conducted an RNA interference–based modifier screen to identify novel regulators of mitosis in Caenorhabditis elegans embryos. Of particular interest, this screen revealed that the Nup205 nucleoporin NPP-3 can negatively modulate the timing of mitotic onset. Furthermore, we discovered that NPP-3 and nucleoporins that are associated with it are lost from the nuclear envelope (NE) in the vicinity of centrosomes at the onset of mitosis. We demonstrate that centrosomes are both necessary and sufficient for NPP-3 local loss, which also requires the activity of the Aurora-A kinase AIR-1. Our findings taken together support a model in which centrosomes and AIR-1 promote timely onset of mitosis by locally removing NPP-3 and associated nucleoporins from the NE.

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

Genetics ◽  
1988 ◽  
Vol 120 (2) ◽  
pp. 423-434
Author(s):  
A M Bullerjahn ◽  
D L Riddle
Keyword(s):  
Fine Structure ◽  
Caenorhabditis Elegans ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Essential Gene ◽  
Resistance Mutation ◽  
Lethal Mutation ◽  
Intragenic Recombination ◽  
Lethal Mutations ◽  
Binding Subunit

Abstract 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.

scholarly journals The IDR-containing protein PID-2 affects Z granules and is required for piRNA-induced silencing in the embryo

2020 ◽  
Author(s):  
Maria Placentino ◽  
António Miguel de Jesus Domingues ◽  
Jan Schreier ◽  
Sabrina Dietz ◽  
Svenja Hellmann ◽  
...  
Keyword(s):  
Gene Regulation ◽  
Caenorhabditis Elegans ◽  
Rna Polymerase ◽  
Small Rna ◽  
Rna Silencing ◽  
Rna Dependent Rna Polymerase ◽  
Prolyl Aminopeptidase ◽  
C Elegans

AbstractIn Caenorhabditis elegans, the piRNA (21U RNA) pathway is required to establish proper gene regulation and an immortal germline. To achieve this, PRG-1-bound 21U RNAs trigger silencing mechanisms mediated by RNA-dependent RNA polymerase (RdRP)-synthetized 22G RNAs. This silencing can become PRG-1-independent, and heritable over many generations. This state is named RNAe. It is unknown how and when RNAe is established, and how it is maintained. We show that maternally provided 21U RNAs can be sufficient to trigger RNAe in embryos. Additionally, we identify the IDR-containing protein PID-2, as a factor required to establish and maintain RNAe. PID-2 interacts with two novel, partially redundant, eTudor domain proteins, PID-4 and PID-5. Additionally, PID-5 has a domain related to the X-prolyl aminopeptidase protein APP-1, and binds APP-1, implicating N-terminal proteolysis in RNAe. All three proteins are required for germline immortality, localize to perinuclear foci, affect Z granules, and are required for balancing of 22G RNA populations. Overall, our study identifies three new proteins with crucial functions in the C. elegans small RNA silencing network.

scholarly journals HCP-4/CENP-C Promotes the Prophase Timing of Centromere Resolution by Enabling the Centromere Association of HCP-6 in Caenorhabditis elegans

2005 ◽  
Vol 25 (7) ◽  
pp. 2583-2592 ◽  
Author(s):  
Landon L. Moore ◽  
Gerald Stanvitch ◽  
Mark B. Roth ◽  
David Rosen
Keyword(s):  
Rna Interference ◽  
Caenorhabditis Elegans ◽  
Holocentric Chromosomes ◽  
Kinetochore Protein ◽  
C Elegans ◽  
Kinetochore Assembly ◽  
Centromere Protein ◽  
Sister Centromere ◽  
Microtubule Capture

ABSTRACT Prior to microtubule capture, sister centromeres resolve from one another, coming to rest on opposite surfaces of the condensing chromosome. Subsequent assembly of sister kinetochores at each sister centromere generates a geometry favorable for equal levels of segregation of chromatids. The holocentric chromosomes of Caenorhabditis elegans are uniquely suited for the study of centromere resolution and subsequent kinetochore assembly. In C. elegans, only two proteins have been identified as being necessary for centromere resolution, the kinase AIR-2 (prophase only) and the centromere protein HCP-4/CENP-C. Here we found that the loss of proteins involved in chromosome cohesion bypassed the requirement for HCP-4/CENP-C but not for AIR-2. Interestingly, the loss of cohesin proteins also restored the localization of HCP-6 to the kinetochore. The loss of the condensin II protein HCP-6 or MIX-1/SMC2 impaired centromere resolution. Furthermore, the loss of HCP-6 or MIX-1/SMC2 resulted in no centromere resolution when either nocodazole or RNA interference (RNAi) of the kinetochore protein KNL-1 perturbed spindle-kinetochore interactions. This result suggests that normal prophase centromere resolution is mediated by condensin II proteins, which are actively recruited to sister centromeres to mediate the process of resolution.

Characterization and expression of a spliced leader RNA in the parasitic nematode Ascaris lumbricoides var. suum

1989 ◽  
Vol 9 (8) ◽  
pp. 3543-3547
Author(s):  
T W Nilsen ◽  
J Shambaugh ◽  
J Denker ◽  
G Chubb ◽  
C Faser ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Secondary Structure ◽  
Rna Polymerase ◽  
Binding Site ◽  
Rna Polymerase Ii ◽  
Ascaris Lumbricoides ◽  
Parasitic Nematode ◽  
Secondary Structures ◽  
Spliced Leader ◽  
C Elegans

The parasitic nematode Ascaris spp. contains a 22-nucleotide spliced-leader (SL) sequence identical to the trans-SL previously described in Caenorhabditis elegans and other nematodes. The SL comprises the first 22 nucleotides of a approximately 110-base RNA and is transcribed by RNA polymerase II. The SL RNA contains a trimethylguanosine cap and a consensus Sm binding site. Furthermore, the Ascaris SL RNA has the potential to adopt a secondary structure which is nearly identical to potential secondary structures of similar SL RNAs in C. elegans and Brugia malayi.

scholarly journals Tissue-Specific Transcription Footprinting Using RNA PoI DamID (RAPID) in Caenorhabditis elegans

Genetics ◽  
2020 ◽  
Vol 216 (4) ◽  
pp. 931-945 ◽  
Author(s):  
Georgina Gómez-Saldivar ◽  
Jaime Osuna-Luque ◽  
Jennifer I. Semple ◽  
Dominique A. Glauser ◽  
Sophie Jarriault ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Rna Polymerase ◽  
Cell Types ◽  
Neuroendocrine Cells ◽  
Cell Physiology ◽  
Specific Gene ◽  
Cell Content ◽  
Tissue Specific ◽  
C Elegans ◽  
Active Transcription

Differential gene expression across cell types underlies development and cell physiology in multicellular organisms. Caenorhabditis elegans is a powerful, extensively used model to address these biological questions. A remaining bottleneck relates to the difficulty to obtain comprehensive tissue-specific gene transcription data, since available methods are still challenging to execute and/or require large worm populations. Here, we introduce the RNA Polymerase DamID (RAPID) approach, in which the Dam methyltransferase is fused to a ubiquitous RNA polymerase subunit to create transcriptional footprints via methyl marks on the DNA of transcribed genes. To validate the method, we determined the polymerase footprints in whole animals, in sorted embryonic blastomeres and in different tissues from intact young adults by driving tissue-specific Dam fusion expression. We obtained meaningful transcriptional footprints in line with RNA-sequencing (RNA-seq) studies in whole animals or specific tissues. To challenge the sensitivity of RAPID and demonstrate its utility to determine novel tissue-specific transcriptional profiles, we determined the transcriptional footprints of the pair of XXX neuroendocrine cells, representing 0.2% of the somatic cell content of the animals. We identified 3901 candidate genes with putatively active transcription in XXX cells, including the few previously known markers for these cells. Using transcriptional reporters for a subset of new hits, we confirmed that the majority of them were expressed in XXX cells and identified novel XXX-specific markers. Taken together, our work establishes RAPID as a valid method for the determination of RNA polymerase footprints in specific tissues of C. elegans without the need for cell sorting or RNA tagging.

scholarly journals Maternal Caffeine Intake Disrupts Eggshell Integrity and Retards Larval Development by Reducing Yolk Production in a Caenorhabditis elegans Model

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1334 ◽  
Author(s):  
Hyemin Min ◽  
Esther Youn ◽  
Yhong-Hee Shim
Keyword(s):  
Growth Rate ◽  
Transcription Factor ◽  
Rna Interference ◽  
Caenorhabditis Elegans ◽  
Larval Development ◽  
Caffeine Intake ◽  
Young Mother ◽  
Psychoactive Substance ◽  
Intergenerational Effects ◽  
F2 Generation

During pregnancy, most women are exposed to caffeine, which is a widely consumed psychoactive substance. However, the consequences of maternal caffeine intake on the child remain largely unknown. Here, we investigated the intergenerational effects of maternal caffeine intake on offspring in a Caenorhabditis elegans model. We treated a young mother (P0) with 10 mM of caffeine equivalent to 2–5 cans of commercial energy drinks and examined its reproduction and growth rate from P0 to F2 generation. The fertility decreased and embryonic lethality increased by defective oocytes and eggshell integrity in caffeine-ingested mothers, and F1 larval development severely retarded. These results were due to decreased production of vitellogenin protein (yolk) in caffeine-ingested mothers. Furthermore, effects of RNA interference of vitellogenin (vit) genes, vit-1 to vit-6, in P0 mothers can mimic those by caffeine-ingested mothers. In addition, RNA interference (RNAi) depletion of unc-62 (human Meis homeobox), a transcriptional activator for vit genes, also showed similar effects induced by caffeine intake. Taken together, maternal caffeine intake reduced yolk production mediated by the UNC-62 transcription factor, thereby disrupting oocyte and eggshell integrity and retarding larval development. Our study suggests the clinical significance of caffeine intake for prospective mothers.

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