Radioadaptive Response for Reproductive Cell Death Demonstrated in In Vivo Tissue Model of Caenorhabditis elegans

2016 ◽  
Vol 185 (4) ◽  
pp. 402 ◽  
Author(s):  
Huangqi Tang ◽  
Liangwen Chen ◽  
Jialu Liu ◽  
Jue Shi ◽  
Qingqing Li ◽  
...  
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Tissue Model ◽  
Reproductive Cell ◽  
Reproductive Cell Death

scholarly journals A Caenorhabditis elegans tissue model of radiation-induced reproductive cell death

2006 ◽  
Vol 103 (26) ◽  
pp. 9946-9951 ◽  
Author(s):  
J. B. Weidhaas ◽  
D. M. Eisenmann ◽  
J. M. Holub ◽  
S. V. Nallur
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Tissue Model ◽  
Reproductive Cell ◽  
Radiation Induced ◽  
Reproductive Cell Death

scholarly journals An in vivo tissue-model of mitotic cell death and EGFR-signaling

2003 ◽  
Vol 57 (2) ◽  
pp. S293
Author(s):  
J.B Weidhaas ◽  
J Holub ◽  
S Leibel ◽  
Z Fuks ◽  
D Eisenmann ◽  
...  
Keyword(s):  
Cell Death ◽  
Mitotic Cell ◽  
Egfr Signaling ◽  
Tissue Model

scholarly journals Ionizing Radiation Induces Delayed Hyperrecombination in Mammalian Cells

2004 ◽  
Vol 24 (11) ◽  
pp. 5060-5068 ◽  
Author(s):  
Lei Huang ◽  
Suzanne Grim ◽  
Leslie E. Smith ◽  
Perry M. Kim ◽  
Jac A. Nickoloff ◽  
...  
Keyword(s):  
Cell Death ◽  
Ionizing Radiation ◽  
Genomic Instability ◽  
Mammalian Cells ◽  
Chromosomal Instability ◽  
Radiation Risk ◽  
Green Fluorescence Protein ◽  
Initial Exposure ◽  
Reproductive Cell ◽  
Reproductive Cell Death

ABSTRACT Exposure to ionizing radiation can result in delayed effects that can be detected in the progeny of an irradiated cell multiple generations after the initial exposure. These effects are described under the rubric of radiation-induced genomic instability and encompass multiple genotoxic endpoints. We have developed a green fluorescence protein (GFP)-based assay and demonstrated that ionizing radiation induces genomic instability in human RKO-derived cells and in human hamster hybrid GM10115 cells, manifested as increased homologous recombination (HR). Up to 10% of cells cultured after irradiation produce mixed GFP+/− colonies indicative of delayed HR or, in the case of RKO-derived cells, mutation and deletion. Consistent with prior studies, delayed chromosomal instability correlated with delayed reproductive cell death. In contrast, cells displaying delayed HR showed no evidence of delayed reproductive cell death, and there was no correlation between delayed chromosomal instability and delayed HR, indicating that these forms of genome instability arise by distinct mechanisms. Because delayed hyperrecombination can be induced at doses of ionizing radiation that are not associated with significantly reduced cell viability, these data may have important implications for assessment of radiation risk and understanding the mechanisms of radiation carcinogenesis.

scholarly journals Mutational Analysis of the Caenorhabditis elegans Cell-Death Gene ced-3

Genetics ◽  
1999 ◽  
Vol 153 (4) ◽  
pp. 1655-1671
Author(s):  
Shai Shaham ◽  
Peter W Reddien ◽  
Brian Davies ◽  
H Robert Horvitz
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Programmed Cell Death ◽  
Mutational Analysis ◽  
Acid Sites ◽  
Site Directed Mutagenesis ◽  
Missense Mutations ◽  
Active Site Cysteine ◽  
Related Proteins

Abstract Mutations in the gene ced-3, which encodes a protease similar to interleukin-1β converting enzyme and related proteins termed caspases, prevent programmed cell death in the nematode Caenorhabditis elegans. We used site-directed mutagenesis to demonstrate that both the presumptive active-site cysteine of the CED-3 protease and the aspartate residues at sites of processing of the CED-3 proprotein are required for programmed cell death in vivo. We characterized the phenotypes caused by and the molecular lesions of 52 ced-3 alleles. These alleles can be ordered in a graded phenotypic series. Of the 30 amino acid sites altered by ced-3 missense mutations, 29 are conserved with at least one other caspase, suggesting that these residues define sites important for the functions of all caspases. Animals homozygous for the ced-3(n2452) allele, which is deleted for the region of the ced-3 gene that encodes the protease domain, seemed to be incompletely blocked in programmed cell death, suggesting that some programmed cell death can occur independently of CED-3 protease activity.

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