Aging

Takagi, Yoshiomi

doi:10.1007/978-3-642-73086-3_9

Cited by 17 publications

(15 citation statements)

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“…Mactys; 9, 66 days; 10, ronuclear DNA damage has been proposed previously to robed with a 32p cause clonal aging in Paramecium (8,9,18). Previous work igonucleotide.…”

Section: Methodsmentioning

confidence: 99%

“…A more specific model for the limited life span of dividing cells has been proposed to be gradual shortening of telomeres, leading eventually to impaired chromosome maintenance (3-6). The ciliated protozoan Paramecium has been studied extensively as a model for clonal cellular aging (7)(8)(9) (12). Telomerase is a specialized cellular reverse transcriptase that synthesizes one strand of telomeric DNA, using as the template a short sequence in the telomerase RNA (13).…”

Section: Introductionmentioning

confidence: 99%

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Lack of telomere shortening during senescence inParamecium.

Gilley

Blackburn

1994

Proc. Natl. Acad. Sci. U.S.A.

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Paramecium terurelia cells have a limited clonal life span and die after -200 fissions if they do not undergo the process of autogamy or coijugation. To test the possibility that cellular senescence of this species is caused by telomere shortening, we analyzed the genomic DNA of the macronucleus during the clonal life span of P. tetwrelia. We found that telomeric DNA sequences were not shortened during the interval of decreased fission rate and cellular death, defined as senescence in these cells. However, the mean size of the macronuclear DNA was markedly decreased during the clonal life span. We present a model that expands upon previous proposals that accumulated DNA damage causes cellular senescence in P. tetraurelia.Cellular and organismal aging have been correlated with accumulated DNA damage (1,2). A more specific model for the limited life span of dividing cells has been proposed to be gradual shortening of telomeres, leading eventually to impaired chromosome maintenance (3-6). The ciliated protozoan Paramecium has been studied extensively as a model for clonal cellular aging (7)(8)(9) (12). Telomerase is a specialized cellular reverse transcriptase that synthesizes one strand of telomeric DNA, using as the template a short sequence in the telomerase RNA (13).One particular telomerase RNA mutation caused telomere shortening and cell death after several cell divisions (12). This result showed that normal telomerase function is required for telomere maintenance and complete replication. Similarly, in the yeast Saccharomyces cerevisiae, mutations of the EST] gene cause progressive telomere shortening and cell death (5). In human tissues and derived cell lines, telomere shortening has been observed to correlate with increasing numbers of cell fissions undergone and has also been proposed to contribute to senescence, although a direct causal relationship has not been demonstrated (6).A distinction exists between the senescence observed with both human cells in culture and Paramecium and the limited clonal life span imposed by mutations causing loss of telomere maintenance in yeast and Tetrahymena. In the former case, senescence is gradual (14), with cell fission rates continuously declining for many divisions before loss of the ability to divide. In contrast, in estl -yeast and Tetrahymena cells that fail to maintain telomeres because of certain mutations in the telomerase RNA, the loss of division capability is relatively precipitous and is not preceded by a gradual decline in fission rate (5,12).We tested the possibility that cellular aging in P. tetraurelia is caused by telomere shortening in the macronucleus. Our analysis of macronuclear DNA shows that shortening of telomeric DNA sequences was not associated with the decreasing fission rates and eventual cell death during the course of the clonal life span of P. tetraurelia. However, we found that the mean size of macronuclear DNA was dramatically decreased during aging. A model is presented in which it is proposed that aberrant repair and consequ...

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“…Mactys; 9, 66 days; 10, ronuclear DNA damage has been proposed previously to robed with a 32p cause clonal aging in Paramecium (8,9,18). Previous work igonucleotide.…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Lack of telomere shortening during senescence inParamecium.

Gilley

Blackburn

1994

Proc. Natl. Acad. Sci. U.S.A.

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“…Conjugation or autogamy resets the clonal life to time zero to initiate the new life cycle from immaturity or autogamy-immaturity. The length of each life cycle stage is counted by the number of fissions, rather than by the physical time (Takagi, 1988). Paramecium that has long been a model organism for cellular aging and clonal lifespan (Sonneborn, 1954(Sonneborn, , 1974Smith-Sonneborn, 1981, 1985Takagi, 1988Takagi, , 1999 proposes fascinating questions such as whether the maximal lifespan could be extended indefinitely or not, what would happen if the immaturity period was drastically shortened or elongated, whether the relationship might exist between the immaturity period and the lifespan, and so forth.…”

Section: Introductionmentioning

confidence: 99%

Novel features of computer-simulated clonal life of Paramecium caudatum

Uezu

Kakutani

Yoshida

et al. 2009

Journal of Theoretical Biology

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The clone of the ciliated protozoan Paramecium caudatum has the immaturity period of about 60 fissions and the lifespan of about 600 fissions. These life cycle figures have been depicted through laboratory experiments that allow continuous cell divisions for hundreds, which never occur in nature. We here constructed the nature-mimicking model culture that alternated the log-and stationary phases to allow conjugation, and computer-simulated the age structure modifying parameters such as cell distributions to start the culture, fission rates, death rates, immaturity periods, probabilities of conjugation, proportions of transplantation and so on. The average and maximum ages in the culture after thousands of alternations were converged to 43 ± 2 and 140 ± 5 fissions, respectively, when parameters for the immaturity period and the maximum clonal lifespan were set at 60 and 600 fissions.This result explains why cells collected in nature are usually young and vigorous.The average and maximum ages proportionally prolonged as the immaturity period was prolonged, as reported true for species of the ciliate. These results indicate the validity of our simulation. The average and maximum ages remained unchanged when the initial condition for starting the culture was changed from two complementary mating-type cells to a population with a quadratic-function * Corresponding author.: +81 742 20 3382: fax: +81 742 20 3382 E-mail address: uezu@cc.nara-wu.ac.jp 1 distribution, and when the fission rate at the log-phase and the death rate at the stationary phase were modified for older ages. The average and maximum ages changed slightly when either the conjugation rate or the proportion of transplantation was somewhat lowered. Although they changed considerably when such parameters as the immaturity period, conjugation rate and death rate were extremely modified, no clones with the age over 230 fissions appeared in any simulations. These results indicate the robustness of the model, which provides us with fresh insight into the structural system of the clonal lifespan of P. caudatum in nature.

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“…The length of sexual immaturity (including interautogamous intervals called autogamy immaturity) is also determined by the number of fissions (see Takagi, 1988). There is a possibility that the biological time by the number of fissions is actually the number of DNA replications in macronucleus (Mikami & Koizumi, 1983).…”

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confidence: 99%

My Paramecium Study, Retrospect and Prospect

Hiwatashi

2001

Zoological Science

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Aging

Cited by 17 publications

References 50 publications

Lack of telomere shortening during senescence inParamecium.

Lack of telomere shortening during senescence inParamecium.

Novel features of computer-simulated clonal life of Paramecium caudatum

My Paramecium Study, Retrospect and Prospect

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