scholarly journals Identification of a gene that shortens clonal life span of Paramecium tetraurelia.

Genetics ◽  
1989 ◽  
Vol 123 (4) ◽  
pp. 749-754 ◽  
Author(s):  
Y Takagi ◽  
K Izumi ◽  
H Kinoshita ◽  
T Yamada ◽  
K Kaji ◽  
...  
Keyword(s):  
Cell Division ◽  
Life Span ◽  
Recessive Mutation ◽  
Supporting Evidence ◽  
Paramecium Tetraurelia ◽  
Wild Type ◽  
Fission Rate ◽  
Cellular Life ◽  
Controlling Mechanism ◽  
Pleiotropic Gene

Abstract We have isolated a Paramecium tetraurelia mutant that divides slowly in daily reisolation cultures and repeats short clonal life spans after successive autogamies. Here we show, using breeding analysis, that a recessive mutation is responsible for the low fission rate and that this low rate is closely related to the short clonal life span. We conclude that a single pleiotropic gene controls these traits and have named it jumyo. In an attempt to further characterize the jumyo mutant, we have revealed that it has a culture life span similar to that of the wild-type cells and that, when mass cultured, it can divide as rapidly as wild-type cells. There was strong evidence that the mutant cells excreted into culture medium some substance that promotes their cell division. These findings may not only present supporting evidence for the hypothesis that the cellular life span is genetically programmed but also give a material basis for the study of the controlling mechanism of cell division in relation to the clonal life span.

scholarly journals Genetic analysis of morphogenetic processes in Paramecium: I. A mutation affecting trichocyst formation and nuclear division

1976 ◽  
Vol 27 (2) ◽  
pp. 109-122 ◽  
Author(s):  
Françoise Ruiz ◽  
André Adoutte ◽  
Michèle Rossignol ◽  
Janine Beisson
Keyword(s):  
Structural Changes ◽  
Nuclear Division ◽  
Pleiotropic Effect ◽  
Recessive Mutation ◽  
Cortical Region ◽  
Paramecium Tetraurelia ◽  
Wild Type ◽  
Nuclear Reorganization ◽  
Nuclear Processes ◽  
Late Stages

SUMMARYMutation tam38 of Paramecium tetraurelia is a nuclear recessive mutation with a pleiotropic effect on both trichocyst morphogenesis and nuclear processes. The analysis of the defective nuclear processes (micronuclear and macronuclear divisions, nuclear reorganization at autogamy) shows that these defects result from an abnormal localization of the nuclei. Phenocopies of tam38 abnormalities can be obtained by vinblastine treatment of wild-type cells at late stages of division. Taking into account the similarity between tam38 and a series of other mutations which also prevent trichocyst attachment to the cell surface and disturb nuclear divisions, the following interpretation is proposed: the absence of attached trichocyst induces structural changes in the plasma membrane or in the cortical region which disturb the normal cortical control of the localization of nuclei.

scholarly journals Selection and analysis of a mutant Paramecium tetraurelia lacking behavioural response to tetraethylammonium

1976 ◽  
Vol 27 (2) ◽  
pp. 97-107 ◽  
Author(s):  
Sheng-Yung Chang ◽  
Ching Kung
Keyword(s):  
Channel Blocker ◽  
Behavioural Response ◽  
Recessive Mutation ◽  
Paramecium Tetraurelia ◽  
Wild Type ◽  
Genetic Analyses ◽  
Behavioural Reaction ◽  
Membrane Defects

SUMMARYWe selected a mutant Paramecium tetraurelia which does not exhibit avoiding reaction in solutions of tetraethylammonium (TEA+), a known membrane K+-channel blocker. Behavioural reaction of the mutant to Na+ solutions was also weak. The rapid successions of avoiding reactions in Ba2+ solutions were observed in both wild type and the TEA-insensitive mutant. Formal genetic analyses showed that this mutant is due to a recessive mutation. This mutation is on a gene completely unlinked to and hypostatic in different degrees to the genes for the membrane defects of ‘pawn A’, ‘pawn B’, ‘ts-pawn C’, ‘fast-2’ and ‘paranoiac A’.

Clonal death associated with the number of fissions in Paramecium caudatum

1980 ◽  
Vol 41 (1) ◽  
pp. 177-191 ◽  
Author(s):  
Y. Takagi ◽  
M. Yoshida
Keyword(s):  
Cell Division ◽  
Life Span ◽  
Morphological Abnormality ◽  
Paramecium Caudatum ◽  
Fission Rate ◽  
Maximal Life Span ◽  
Original Clone

Contrary to an earlier report suggesting clonal immortality in Paramecium caudatum, the clones of the same species in this study terminated inevitably with a maximal life-span of 658 fissions and showed, prior to clonal death, decreased fission rate, increased probability of the appearance of non-dividing or dead cells after cell division, and increased frequency of morphological abnormality and of division asynchrony. Clonal senescence and death after a limited number of fissions was reproducible even if subclones derived from the original clone of a known fission age were examined again after a lag of 468 days. These results indicate that clones of P. caudatum are mortal and that they use fissions, not days, to measure life-span. Possible causes for the discrepancies between the earlier report and the present one are discussed.

Uncoupling of basal body duplication and cell division in crochu, a mutant of Paramecium hypersensitive to nocodazole

Development ◽  
1998 ◽  
Vol 125 (7) ◽  
pp. 1305-1314
Author(s):  
M. Jerka-Dziadosz ◽  
F. Ruiz ◽  
F. Beisson
Keyword(s):  
Cell Division ◽  
Basal Body ◽  
Cell Shape ◽  
Surface Pattern ◽  
Recessive Mutation ◽  
Basal Bodies ◽  
Wild Type ◽  
In The Wild ◽  
Cortical Cytoskeleton ◽  
Do So

In Paramecium the development of cell shape and surface pattern during division depends on a precise spatial and temporal pattern of duplication of the ciliary basal bodies which are the organizers of the cortical cytoskeleton. According to their localization, basal bodies will duplicate once, more than once or not all and this duplication is coupled with cell division, as is centrosomal duplication in metazoan cells. We describe here a monogenic nuclear recessive mutation, crochu1 (cro1), resulting in abnormal cell shape and cortical pattern and hypersensitivity to nocodazole. The cytological analysis, by immunofluorescence and electron microscopy, demonstrates that the mutation causes hyper duplication of basal bodies and releases both spatial and temporal control of duplication as basal bodies continue to proliferate in interphase and do so at ectopic locations, beneath the surface and in cortical territories where no duplication occurs in the wild type. However, the abnormal surface organization of cro1 cells does not affect the program of basal body duplication during division. By genetic analysis, no interaction was detected with the sm19 mutation which impairs basal body duplication. In contrast, the cro1 mutation suppresses the nocodazole resistance conferred by nocr1, a mutation in a beta-tubulin gene. This interaction suggests that the primary effect of the mutation bears on microtubule dynamics, whose instability, normally increased during division, would persist throughout the interphase and provide a signal for constitutive basal body duplication.

scholarly journals Regeneration of the Eyespot and Flagellum in Euglena gracilis during Cell Division

Plants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2004
Author(s):  
Kazunari Ozasa ◽  
Hyunwoong Kang ◽  
Simon Song ◽  
Shun Tamaki ◽  
Tomoko Shinomura ◽  
...  
Keyword(s):  
Cell Division ◽  
Life Span ◽  
Euglena Gracilis ◽  
Live Cell Imaging ◽  
Cell Tracking ◽  
Cell Imaging ◽  
Early Stage ◽  
Single Cells ◽  
Wild Type ◽  
Daughter Cells

Cell division of unicellular microalgae is a fascinating process of proliferation, at which whole organelles are regenerated and distributed to two new lives. We performed dynamic live cell imaging of Euglena gracilis using optical microscopy to elucidate the mechanisms involved in the regulation of the eyespot and flagellum during cell division and distribution of the organelles into the two daughter cells. Single cells of the wild type (WT) and colorless SM-ZK cells were confined in a microfluidic device, and the appearance of the eyespot (stigma) and emergent flagellum was tracked in sequential video-recorded images obtained by automatic cell tracking and focusing. We examined 12 SM-ZK and 10 WT cells and deduced that the eyespot diminished in size and disappeared at an early stage of cell division and remained undetected for 26–97 min (62 min on average, 22 min in deviation). Subsequently, two small eyespots appeared and were distributed into the two daughter cells. Additionally, the emergent flagellum gradually shortened to zero-length, and two flagella emerged from the anterior ends of the daughter cells. Our observation revealed that the eyespot and flagellum of E. gracilis are degraded once in the cell division, and the carotenoids in the eyespot are also decomposed. Subsequently, the two eyespots/flagella are regenerated for distribution into daughter cells. As a logical conclusion, the two daughter cells generated from a single cell division possess the equivalent organelles and each E. gracilis cell has eternal or non-finite life span. The two newly regenerated eyespot and flagellum grow at different rates and mature at different timings in the two daughter cells, resulting in diverse cell characteristics in E. gracilis.

scholarly journals The Cloning and Molecular Analysis of pawn-B in Paramecium tetraurelia

Genetics ◽  
2000 ◽  
Vol 155 (3) ◽  
pp. 1105-1117 ◽  
Author(s):  
W John Haynes ◽  
Kit-Yin Ling ◽  
Robin R Preston ◽  
Yoshiro Saimi ◽  
Ching Kung
Keyword(s):  
Genomic Library ◽  
Open Reading Frame ◽  
Paramecium Tetraurelia ◽  
Wild Type ◽  
Rt Pcr ◽  
Reading Frame ◽  
Close Proximity ◽  
In The Wild ◽  
Dna Fragment ◽  
Alternative Sites

Abstract Pawn mutants of Paramecium tetraurelia lack a depolarization-activated Ca2+ current and do not swim backward. Using the method of microinjection and sorting a genomic library, we have cloned a DNA fragment that complements pawn-B (pwB/pwB). The minimal complementing fragment is a 798-bp open reading frame (ORF) that restores the Ca2+ current and the backward swimming when expressed. This ORF contains a 29-bp intron and is transcribed and translated. The translated product has two putative transmembrane domains but no clear matches in current databases. Mutations in the available pwB alleles were found within this ORF. The d4-95 and d4-96 alleles are single base substitutions, while d4-662 (previously pawn-D) harbors a 44-bp insertion that matches an internal eliminated sequence (IES) found in the wild-type germline DNA except for a single C-to-T transition. Northern hybridizations and RT-PCR indicate that d4-662 transcripts are rapidly degraded or not produced. A second 155-bp IES in the wild-type germline ORF excises at two alternative sites spanning three asparagine codons. The pwB ORF appears to be separated from a 5′ neighboring ORF by only 36 bp. The close proximity of the two ORFs and the location of the pwB protein as indicated by GFP-fusion constructs are discussed.

scholarly journals Genetic, Behavioral and Environmental Determinants of Male Longevity in Caenorhabditis elegans

Genetics ◽  
2000 ◽  
Vol 154 (4) ◽  
pp. 1597-1610 ◽  
Author(s):  
David Gems ◽  
Donald L Riddle
Keyword(s):  
Caenorhabditis Elegans ◽  
Life Span ◽  
Wild Type ◽  
Neuronal Function ◽  
Nematode Caenorhabditis Elegans ◽  
Wild Isolate ◽  
Young Males ◽  
C Elegans ◽  
Single Sex ◽  
Solitary Males

Abstract Males of the nematode Caenorhabditis elegans are shorter lived than hermaphrodites when maintained in single-sex groups. We observed that groups of young males form clumps and that solitary males live longer, indicating that male-male interactions reduce life span. By contrast, grouped or isolated hermaphrodites exhibited the same longevity. In one wild isolate of C. elegans, AB2, there was evidence of copulation between males. Nine uncoordinated (unc) mutations were used to block clumping behavior. These mutations had little effect on hermaphrodite life span in most cases, yet many increased male longevity even beyond that of solitary wild-type males. In one case, the neuronal function mutant unc-64(e246), hermaphrodite life span was also increased by up to 60%. The longevity of unc-4(e120), unc-13(e51), and unc-32(e189) males exceeded that of hermaphrodites by 70–120%. This difference appears to reflect a difference in sex-specific life span potential revealed in the absence of male behavior that is detrimental to survival. The greater longevity of males appears not to be affected by daf-2, but is influenced by daf-16. In the absence of male-male interactions, median (but not maximum) male life span was variable. This variability was reduced when dead bacteria were used as food. Maintenance on dead bacteria extended both male and hermaphrodite longevity.

scholarly journals Mitochondrial Group II Introns, Cytochrome c Oxidase, and Senescence in Podospora anserina

1999 ◽  
Vol 19 (6) ◽  
pp. 4093-4100 ◽  
Author(s):  
Odile Begel ◽  
Jocelyne Boulay ◽  
Beatrice Albert ◽  
Eric Dufour ◽  
Annie Sainsard-Chanet
Keyword(s):  
Life Span ◽  
Integration Site ◽  
Group Ii Intron ◽  
Podospora Anserina ◽  
Wild Type ◽  
First Intron ◽  
Limited Life ◽  
Related Group ◽  
Group Ii ◽  
Mitochondrial Chromosome

ABSTRACT Podospora anserina is a filamentous fungus with a limited life span. It expresses a degenerative syndrome called senescence, which is always associated with the accumulation of circular molecules (senDNAs) containing specific regions of the mitochondrial chromosome. A mobile group II intron (α) has been thought to play a prominent role in this syndrome. Intron α is the first intron of the cytochrome c oxidase subunit I gene (COX1). Mitochondrial mutants that escape the senescence process are missing this intron, as well as the first exon of theCOX1 gene. We describe here the first mutant of P. anserina that has the α sequence precisely deleted and whose cytochrome c oxidase activity is identical to that of wild-type cells. The integration site of the intron is slightly modified, and this change prevents efficient homing of intron α. We show here that this mutant displays a senescence syndrome similar to that of the wild type and that its life span is increased about twofold. The introduction of a related group II intron into the mitochondrial genome of the mutant does not restore the wild-type life span. These data clearly demonstrate that intron α is not the specific senescence factor but rather an accelerator or amplifier of the senescence process. They emphasize the role that intron α plays in the instability of the mitochondrial chromosome and the link between this instability and longevity. Our results strongly support the idea that in Podospora, “immortality” can be acquired not by the absence of intron α but rather by the lack of active cytochromec oxidase.

scholarly journals Phenotypic and Genetic Analysis of “Chameleon,” a Paramecium Mutant With an Enhanced Sensitivity to Magnesium

Genetics ◽  
1997 ◽  
Vol 146 (3) ◽  
pp. 871-880
Author(s):  
Robin R Preston ◽  
Jocelyn A Hammond
Keyword(s):  
Genetic Analysis ◽  
Single Locus ◽  
Behavioral Analysis ◽  
Paramecium Tetraurelia ◽  
Wild Type ◽  
Ion Conductance ◽  
Membrane Excitation ◽  
Enhanced Sensitivity ◽  
Electrophysiological Analysis ◽  
Mutant Strains

Three mutant strains of Paramecium tetraurelia with an enhanced sensitivity to magnesium have been isolated. These new “Chameleon” mutants result from partial- or codominant mutations at a single locus, Cha. Whereas the wild type responded to 5 mm Mg2+ by swimming backward for 10–15 sec, Cha mutants responded with ∼30 sec backward swimming. Electrophysiological analysis suggested that this behavior may be caused by slowing in the rate at which a Mg2+-specific ion conductance deactivates following membrane excitation. This would be consistent with an observed increase in the sensitivity of Cha mutants to nickel poisoning, since Ni2+ is also able to enter the cell via this pathway. More extensive behavioral analysis showed that Cha cells also overresponded to Na+, but there was no evidence for a defect in intracellular Ca2+ homeostasis that might account for a simultaneous enhancement of both the Mg2+ and Na+ conductances. The possibility that the Cha locus may encode a specific regulator of the Mg2+- and Na+-permeabilities is considered.

scholarly journals Loss of Ubp3 increases silencing, decreases unequal recombination in rDNA, and shortens the replicative life span in Saccharomyces cerevisiae

2014 ◽  
Vol 25 (12) ◽  
pp. 1916-1924 ◽  
Author(s):  
David Öling ◽  
Rehan Masoom ◽  
Kristian Kvint
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Rna Polymerase ◽  
Life Span ◽  
Rna Polymerase Ii ◽  
Ribosomal Dna ◽  
Genetic Evidence ◽  
Wild Type ◽  
Replicative Life Span ◽  
Unequal Recombination

Ubp3 is a conserved ubiquitin protease that acts as an antisilencing factor in MAT and telomeric regions. Here we show that ubp3∆ mutants also display increased silencing in ribosomal DNA (rDNA). Consistent with this, RNA polymerase II occupancy is lower in cells lacking Ubp3 than in wild-type cells in all heterochromatic regions. Moreover, in a ubp3∆ mutant, unequal recombination in rDNA is highly suppressed. We present genetic evidence that this effect on rDNA recombination, but not silencing, is entirely dependent on the silencing factor Sir2. Further, ubp3∆ sir2∆ mutants age prematurely at the same rate as sir2∆ mutants. Thus our data suggest that recombination negatively influences replicative life span more so than silencing. However, in ubp3∆ mutants, recombination is not a prerequisite for aging, since cells lacking Ubp3 have a shorter life span than isogenic wild-type cells. We discuss the data in view of different models on how silencing and unequal recombination affect replicative life span and the role of Ubp3 in these processes.

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