Caffeine-resistant mutants of<i>Caenorhabditis elegans</i>

Hartman, Paul A.

doi:10.1017/s0016672300026896

Cited by 20 publications

(23 citation statements)

References 24 publications

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“…For the most radio-resistant species in the tabulation, the lepidopteran Spilosoma (Diacrasia) obliqua, a dose of 200 Gy to pupal or adult males, the most resistant sex, resulted in Ͼ99% F 1 sterilization. § Among other invertebrates, sensitivity to IR has been measured for Xirradiation of Caenorhabditis elegans eggs in buffer, for which Ϸ30 Gy reduced the number developing into adults by 90% and the snail Zonitoides arboreus, which produced only sterile eggs after exposure to 70 Gy (16,17). Among the very few animal species known to be capable, like bdelloid rotifers, of anhydrobiosis at any life stage, resistance to IR has been studied in the tardigrades Richtersius coronifer and Milnesium tardigradum, which produced only sterile eggs after exposure to the lowest doses tested, 500 and 1,000 Gy, respectively (18,19).…”

Section: Discussionmentioning

confidence: 99%

Extreme resistance of bdelloid rotifers to ionizing radiation

Gladyshev

Meselson

2008

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

240

193

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Rotifers of class Bdelloidea are common invertebrate animals with highly unusual characteristics, including apparently obligate asexuality, the ability to resume reproduction after desiccation at any life stage, and a paucity of transposable genetic elements of types not prone to horizontal transmission. We find that bdelloids are also extraordinarily resistant to ionizing radiation (IR). Reproduction of the bdelloids Adineta vaga and Philodina roseola is much more resistant to IR than that of Euchlanis dilatata, a rotifer belonging to the desiccation-intolerant and facultatively sexual class Monogononta, and all other animals for which we have found relevant data. By analogy with the desiccation-and radiationresistant bacterium Deinococcus radiodurans, we suggest that the extraordinary radiation resistance of bdelloid rotifers is a consequence of their evolutionary adaptation to survive episodes of desiccation encountered in their characteristic habitats and that the damage incurred in such episodes includes DNA breakage that is repaired upon rehydration. Such breakage and repair may have maintained bdelloid chromosomes as colinear pairs and kept the load of transposable genetic elements low and may also have contributed to the success of bdelloid rotifers in avoiding the early extinction suffered by most asexuals.desiccation ͉ DNA repair ͉ asexual reproduction ͉ anhydrobiosis

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Section: Discussionmentioning

confidence: 99%

Extreme resistance of bdelloid rotifers to ionizing radiation

Gladyshev

Meselson

2008

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

240

193

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“…The presence of mrt-2 or hus-1 was assessed by scoring for sterility following gamma irradiation of six L1 larvae per strain at a dose of 60 Gy. The presence of clk-2(mn159) was assessed on the basis of its temperaturesensitive sterile phenotype (Hartman and Herman 1982). The mutation hus-1(op241), which lies on chromosome I, was originally identified in the strain CB1480 him-7(e1480) V (Gartner et al 2000).…”

Section: Methodsmentioning

confidence: 99%

“…Both atl-1 and clk-2 are essential, and a strong defect in either gene results in the accumulation of single-stranded DNA and mitotic failure (GarciaMuse and Boulton 2005). Two conditional mutations of clk-2 have been identified: mn159 was recovered in a screen for radiation-hypersensitive mutants of C. elegans (hence its former gene name ''rad-5'') (Hartman and Herman 1982), and qm37 was identified in a screen for mutations that confer a maternally rescued Slow Growth phenotype (Lakowski and Hekimi 1996).…”

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confidence: 99%

Mutator Phenotype ofCaenorhabditis elegansDNA Damage Checkpoint Mutants

Harris¹,

Lowden²,

Clejan

et al. 2006

Genetics

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DNA damage response proteins identify sites of DNA damage and signal to downstream effectors that orchestrate either apoptosis or arrest of the cell cycle and DNA repair. The C. elegans DNA damage response mutants mrt-2, hus-1, and clk-2(mn159) displayed 8-to 15-fold increases in the frequency of spontaneous mutation in their germlines. Many of these mutations were small-to medium-sized deletions, some of which had unusual sequences at their breakpoints such as purine-rich tracts or direct or inverted repeats. Although DNA-damage-induced apoptosis is abrogated in the mrt-2, hus-1, and clk-2 mutant backgrounds, lack of the apoptotic branch of the DNA damage response pathway in cep-1/p53, ced-3, and ced-4 mutants did not result in a Mutator phenotype. Thus, DNA damage checkpoint proteins suppress the frequency of mutation by ensuring that spontaneous DNA damage is accurately repaired in C. elegans germ cells. Although DNA damage response defects that predispose humans to cancer are known to result in large-scale chromosome aberrations, our results suggest that small-to medium-sized deletions may also play roles in the development of cancer.

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“…43,45,46 All three mutations abrogate cell cycle arrest and apoptosis induced by DNA damage (Figure 2b), without affecting developmental or physiological germ cell death. Consistent with the situation in yeast and mammalian checkpoint gene mutants, they also show increased genomic instability and reduced long-term survival following genotoxic insults, as the high rates of embryonic lethality demonstrate.…”

Section: Checkpoint Mutants In C Elegansmentioning

confidence: 99%

Death and more: DNA damage response pathways in the nematode C. elegans

2003

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Genotoxic stress is a threat to our cells' genome integrity. Failure to repair DNA lesions properly after the induction of cell proliferation arrest can lead to mutations or large-scale genomic instability. Because such changes may have tumorigenic potential, damaged cells are often eliminated via apoptosis. Loss of this apoptotic response is actually one of the hallmarks of cancer. Towards the effort to elucidate the DNA damage-induced signaling steps leading to these biological events, an easily accessible model system is required, where the acquired knowledge can reveal the mechanisms underlying more complex organisms. Accumulating evidence coming from studies in Caenorhabditis elegans point to its usefulness as such. In the worm's germline, DNA damage can induce both cell cycle arrest and apoptosis, two responses that are spatially separated. The latter is a tightly controlled process that is genetically indistinguishable from developmental programmed cell death. Upstream of the central death machinery, components of the DNA damage signaling cascade lie and act either as sensors of the lesion or as transducers of the initial signal detected. This review summarizes the findings of several studies that specify the elements of the DNA damage-induced responses, as components of the cell cycle control machinery, the repairing process or the apoptotic outcome. The validity of C. elegans as a tool to further dissect the complex signaling network of these responses and the high potential for it to reveal important links to cancer and other genetic abnormalities are addressed.

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Caffeine-resistant mutants ofCaenorhabditis elegans

Cited by 20 publications

References 24 publications

Extreme resistance of bdelloid rotifers to ionizing radiation

Extreme resistance of bdelloid rotifers to ionizing radiation

Mutator Phenotype ofCaenorhabditis elegansDNA Damage Checkpoint Mutants

Death and more: DNA damage response pathways in the nematode C. elegans

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