Cocultivation of Fanconi Anemia Cells and of Mouse Lymphoma Mutants Leads to Interspecies Complementation of Chromosomal Hypersensitivity to DNA Cross-linking Agents

Overview

Journal Hum Genet

Specialty Genetics

Date 1990 May 1

PMID 2110930

Citations 3

Authors

F Rosselli

E MOUSTACCHI

Affiliations

Soon will be listed here.

Abstract

We have studied the effects of cocultivation on the frequency of mitomycin C (MMC)-induced chromosomal aberrations. This was carried out by cocultivating Fanconi anemia (FA) cells from the genetic complementation groups A and B with both normal mouse lymphoma L5178Y cells and the derived "FA-like" mutant cells, MCN-151 and MCE-50, assigned to complementation groups I and II, respectively. The results show a partial complementation of the defect (i.e. a reduction in the frequency of chromosomal aberration) in FA group A cells cocultured with normal or group II mouse cells, and a partial correction of mouse group I cells cocultived with normal or FA group B human cells. No reciprocal effects were observed between FA group A cells and mouse group I mutant cells; the frequencies of MMC-induced chromosomal aberrations in these cells remained unchanged by cocultivation. Moreover, no complementation was observed for both FA group B cells and mouse group II cells, after cocultivation with normal cells of either mouse or human origin. This implies that a diffusible factor released by normal human and mouse cells, and by FA group B and mouse group II mutant cells, can correct at least in part the chromosomal defect of FA group A and mouse group I mutant cells. With normal human or mouse cells, the frequency of chromosomal breakage after cocultivation remains the same as that observed in non-cocultived cells. This suggests that no detectable clastogenic factor is released by human FA or "FA-like" mouse cells.

Citing Articles

Irreversible repression of DNA synthesis in Fanconi anemia cells is alleviated by the product of a novel cyclin-related gene.

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PMID: 7799938 PMC: 231958. DOI: 10.1128/MCB.15.1.305.

Partial complementation of the Fanconi anemia defect upon transfection by heterologous DNA. Phenotypic dissociation of chromosomal and cellular hypersensitivity to DNA cross-linking agents.

Diatloff-Zito C, Rosselli F, Heddle J, MOUSTACCHI E Hum Genet. 1990; 86(2):151-61.

PMID: 2265827 DOI: 10.1007/BF00197697.

Abnormal lymphokine production: a novel feature of the genetic disease Fanconi anemia. I. Involvement of interleukin-6.

Rosselli F, Sanceau J, Wietzerbin J, MOUSTACCHI E Hum Genet. 1992; 89(1):42-8.

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