Gene mapping of SEZ group genes and determination of pentylenetetrazol susceptible quantitative trait loci in the mouse chromosome

Wakana, Shigeharu; Sugaya, Eiichi; Naramoto, Fumiki; Yokote, Norikazu; Maruyama, Chika; Jin, Wen; Ohguchi, Hiromi; Terada, Tadashi; Sugaya, Akira; Kajiwara, Kagemasa

doi:10.1016/s0006-8993(99)02406-3

Cited by 20 publications

(19 citation statements)

References 18 publications

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“…Wakana and colleagues (2000) confirmed that the C57BL/6J strain is relatively resistant to PTZ treatment, whereas the DBA/2J line is more susceptible to seizure, and the F2 derived recombinant inbred strain, BXD line, display a range of responses to PTZ. More specifically, these data demonstrate that the BXD29/Ty strain exhibit a similar resistance to PTZ induced seizure behavior to the C57BL/6J parental line.…”

Section: Introductionmentioning

confidence: 66%

“…Previous work has demonstrated that the BXD29/Ty strain exhibit a similar threshold for PTZ-induced seizure behavior to the C57BL/6J parental line (Wakana et al 2000). In our study, BXD29/Ty mice also exhibit a similar threshold for PTZ induced seizure behavior in comparison to C57BL/10J mice based on the latency and concentration of PTZ needed to generate myoclonic jerk (i.e.…”

Section: Discussionmentioning

confidence: 93%

“…Examination of the seizure susceptibility of the parental lines, C57BL/6J and DBA/2J, as well as the majority of the first cohort of BXD strains demonstrated the variable resistance to the chemi-convulsant pentylenetetrazole (PTZ) (Wakana et al 2000). Wakana and colleagues (2000) confirmed that the C57BL/6J strain is relatively resistant to PTZ treatment, whereas the DBA/2J line is more susceptible to seizure, and the F2 derived recombinant inbred strain, BXD line, display a range of responses to PTZ.…”

Section: Introductionmentioning

confidence: 99%

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Differential seizure response in two models of cortical heterotopia

et al. 2013

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Malformations of cortical development (MCD) are linked to epilepsy in humans. MCD encompass a broad spectrum of malformations, which occur as the principal pathology or a secondary disruption. Recently, Rosen et al. (2012) reported that BXD29-Trl4lps-2J/J mice have subcortical nodular heterotopias with partial agenesis of the corpus callosum (p-ACC). Additionally Ramos and colleagues (2008) demonstrated that C57BL/10J mice exhibit cortical heterotopias with no additional cortical abnormalities. We examined the seizure susceptibility of these mice to determine if the presence (BXD29-Trl4lps-2J/J) or absence (C57BL/10J) of p-ACC, in strains with MCD, confers a differential response to chemi-convulsive treatment. Our results indicate that C57BL/10J mice with layer I heterotopia are more susceptible, whereas BXD29-Trl4lps-2J/J mice with more severe subcortical nodular heterotopia and p-ACC are more resistant to seizure behavior induced by pentylenetetrazole. These data suggest that p-ACC may confer seizure resistance in models of MCD.

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Section: Introductionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

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Differential seizure response in two models of cortical heterotopia

et al. 2013

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“…Although a large body of data indicates that there are substantial differences in seizure susceptibility induced by chemical or electrical means in different strains that are genetically determined (Ferraro et al, 1995(Ferraro et al, , 1997(Ferraro et al, , 1998(Ferraro et al, , 1999(Ferraro et al, , 2001Wakana et al, 2000), the differences in susceptibility to seizure-induced hippocampal cell death are not related to differences in seizure activity induced by KA (Schauwecker and Steward, 1997). In particular, strains of mice that differ dramatically in the extent of hippocampal neurodegeneration in response to KA nevertheless exhibit the same class of behavioral seizures, and the pattern and extent of neuronal activity are comparable as revealed by 2-deoxyglucose autoradiography (Schauwecker and Steward, 1997).…”

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confidence: 99%

Genetic control of sensitivity to hippocampal cell death induced by kainic acid: A quantitative trait loci analysis

Schauwecker

Williams

Santos

2004

J of Comparative Neurology

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Host genetic factors are likely to contribute to differences in individual susceptibility to seizure-induced excitotoxic neuronal damage. Similarly, inbred strains of mice differ in their susceptibility to the kainic acid (KA) model of seizure-induced cell death, but the genes responsible for the differences are not known. Here, we define the inheritance patterns of susceptibility to KA-induced neurodegeneration in the hippocampus by assessing 331 back-cross (N2) progeny of two inbred mouse strains, C57BL/6 and FVB/N, previously shown to display resistance and sensitivity to KA-induced cell death, respectively. Results of phenotypic analysis suggest that the difference in susceptibility between these two strains is conferred by a single dominant gene. Therefore, we used an N2 back-cross between the inbred C57BL/6 and FVB/N strains for a genome-wide search for quantitative trait loci (QTLs), which are chromosomal sites containing genes influencing the magnitude of susceptibility. Genome-wide interval mapping in N2 progeny identified a locus on distal chromosome (Chr) 18 with a peak LOD score of 4.9 localized between D18Mit186 and D18Mit4 as having the strongest and most significant effect in this model. QTLs of minor effect were detected on Chr 15 (D15Mit174-D15Mit156) and Chr 4 (D4Mit264-D4Mit91), with peak LOD scores of 3.02 and 2.46, respectively. The three significant QTLs (Chrs 4, 15, 18) together account for nearly 25% of the trait variance for both genders combined. Reduced KA-induced cell death susceptibility was observed in a congenic strain in which the highly susceptible FVB/N strain carried putative resistance alleles from the C57BL/6 strain on Chr 18.

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“…Because the heterozygous cells displayed a phenotype of intermediate sensitivity, the levels of Rev3L may determine drug tolerance. In this context, it is important to note that Rev3L is overexpressed in gliomas ) and can presumably be up-regulated upon drug exposure (Wakana et al, 2000). Combined with our finding that Rev3L levels may be rate-limiting in the development of drug tolerance, Rev3L may be a primary determinant in the development of tolerance to alkylating chemotherapy.…”

Section: Downloaded Frommentioning

confidence: 61%

The Translesion Polymerase Rev3L in the Tolerance of Alkylating Anticancer Drugs

Roos¹,

Tsaalbi-Shtylik²,

Tsaryk³

et al. 2009

Mol Pharmacol

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Temozolomide and fotemustine, representing methylating and chloroethylating agents, respectively, are used in the treatment of glioma and malignant melanoma. Because chemoresistance of these tumors is a common phenomenon, identification of the underlying mechanisms is needed. Here we show that Rev3L, the catalytic subunit of the translesion DNA polymerase , mediates resistance to both temozolomide and fotemustine. Rev3L knockout cells are hypersensitive to both agents. It is remarkable that cells heterozygous for Rev3L showed an intermediate sensitivity. Rev3L is not involved in the tolerance of the toxic O 6 -methylguanine lesion. However, a possible role of Rev3L in the tolerance of O 6 -chloroethylguanine or the subsequently formed N1-guanine-N3-cytosine interstrand cross-link is shown. Rev3L had no influence on base excision repair (BER) of the N-alkylation lesions but is very likely to be involved in the tolerance of N-alkylations or apurinic/apyrimidinic sites originating from them. We also show that Rev3L exerts its protective effect in replicating cells and that loss of Rev3L leads to a significant increase in DNA double-strand breaks after temozolomide and fotemustine treatment. These data show that Rev3L contributes to temozolomide and fotemustine resistance, thus acting in concert with O 6

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Gene mapping of SEZ group genes and determination of pentylenetetrazol susceptible quantitative trait loci in the mouse chromosome

Cited by 20 publications

References 18 publications

Differential seizure response in two models of cortical heterotopia

Differential seizure response in two models of cortical heterotopia

Genetic control of sensitivity to hippocampal cell death induced by kainic acid: A quantitative trait loci analysis

The Translesion Polymerase Rev3L in the Tolerance of Alkylating Anticancer Drugs

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