Localization of growth arrest-specific genes on mouse Chromosomes 1, 7, 8, 11, 13, and 16

Colombo, Mario P.; Martinotti, Alessia; Howard, Thad A.; Schneider, Claudio; D’Eustachio, Peter; Seldin, Michael F.

doi:10.1007/bf00353861

Cited by 34 publications

(11 citation statements)

References 26 publications

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“…Recently, the Gas-3 gene was localized to mouse chromosome 11 through a combination of interspecific backcross mapping and recombinant inbred strain analyses (24). Colombo et aL (24) localized Gas-3 7.0 ± 2.4 cM distal to I1-3 (interleukin 3) and 4.4 ± 1.8 cM proximal to TrpS3 (transformation-related protein 53). These results are consistent with the data presented in this report.…”

Section: Identification Of Restriction Fragment Length Polymorphisms mentioning

confidence: 99%

A leucine-to-proline mutation in the putative first transmembrane domain of the 22-kDa peripheral myelin protein in the trembler-J mouse.

Suter

Moskow

Welcher

et al. 1992

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

266

138

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A leucine-to-proline mutation in the putative first transmembrane domain of the 22-kDa peripheral myelin protein in the trembler-J mouse ( ABSTRACTPeripheral myelin protein PMP-22 is a potential growth-regulating myelin protein that is expressed by Schwann cells and predominantly localized in compact peripheral myelin. A point mutation in the Pmp-22 gene of inbred trembler (Tr) mice was identified and proposed to be responsible for the Tr phenotype, which is characterized by paralysis of the limbs as well as tremors and transient seizures. In support of this hypothesis, we now report the fine mapping of the Pmp-22 gene to the immediate vicinity of the Tr locus on mouse chromosome 11. Furthermore, we have found a second point mutation in the Pmp-22 gene of trembler-J (TrJ) mice, which results in the substitution ofa leucine residue by a proline residue in the putative first transmembrane region of the PMP-22 polypeptide. Tr and TrJ were previously mapped

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Section: Identification Of Restriction Fragment Length Polymorphisms mentioning

confidence: 99%

A leucine-to-proline mutation in the putative first transmembrane domain of the 22-kDa peripheral myelin protein in the trembler-J mouse.

Suter

Moskow

Welcher

et al. 1992

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

266

138

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“…The bracket on the right designates the unknown order of Snrpn and ZnfJ27 in the mouse. The placement of the Gas2 locus (22) on this particular panel of deletions, as well as the extent of the p3RD300H deletion, are based on unpublished data from E.M.R. The shaded box represents current uncertainty about the distal extent of the p3RD300H deletion.…”

Section: Resultsmentioning

confidence: 99%

Pleiotropy in microdeletion syndromes: neurologic and spermatogenic abnormalities in mice homozygous for the p6H deletion are likely due to dysfunction of a single gene.

Rinchik

Carpenter²,

Handel³

1995

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

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Variability and complexity of phenotypes observed in microdeletion syndromes can be due to deletion of a single gene whose product participates in several aspects of development or can be due to the deletion of a number of tightly linked genes, each adding its own effect to the syndrome. The p6H deletion in mouse chromosome 7 presents a good model with which to address this question of multigene vs. single-gene pleiotropy. Mice homozygous for the p6H deletion are diluted in pigmentation, are smaller than their littermates, and manifest a nervous jerky-gait phenotype. Male homozygotes are sterile and exhibit profound abnormalities in spermiogenesis. By using N-ethyl-N-nitrosourea (EtNU) mutagenesis and a breeding protocol designed to recover recessive mutations expressed hemizygously opposite a large p-locus deletion, we have generated three noncomplementing mutations that map to thep6H deletion. Each of these EtNU-induced mutations has adverse effects on the size, nervous behavior, and progression of spermiogenesis that characterize p6H deletion homozygotes. Because EtNU is thought to induce primarily intragenic (point) mutations in mouse stem-cell spermatogonia, we propose that the trio of phenotypes (runtiness, nervous jerky gait, and male sterility) expressed in p6H deletion homozygotes is the result of deletion of a single highly pleiotropic gene. We also predict that a homologous single locus, quite possibly tightly linked and distal to the DJSS12 (P) locus in human chromosome 15qll-q13, may be associated with similar developmental abnormalities in humans.

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“…Human and mouse gas1 genes are located in the long arms of chromosome 9 (9q21.3-q22) [50,51] and chromosome 13 [52] respectively, with 77.04% of homology between them. Gas1 is an intronless gene, suggesting that it probably originated from a retrotransposon.…”

Section: Transcriptional and Translational Regulationmentioning

confidence: 99%

Effects of Gas1 on gliomas: a review on current preclinical studies

Segovia¹,

Bautista²,

Lara-Lozano³

2016

JCMT

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Glioblastoma multiforme (GBM) is the most common and lethal brain tumor. Its prognosis remains very poor, despite the use of combined treatments such as surgical resection, radiation and chemotherapy. The major limitations for the treatment of GBM are its high invasiveness, tumor recurrence and resistance to treatments. Therefore, gene therapy appears as a relevant strategy for its treatment. Thus, we have investigated the use of growth-arrest-specific 1 (Gas1) for the treatment of GBM. Gas1 is a tumor suppressor protein that inhibits glioma growth by inducing arrest and apoptosis of tumor cells. Moreover, we have shown that a soluble form of Gas1 acting in both autocrine and paracrine manners is also effective inhibiting tumor growth in animal models, indicating its potential as an adjuvant for the treatment of GBM.

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Localization of growth arrest-specific genes on mouse Chromosomes 1, 7, 8, 11, 13, and 16

Cited by 34 publications

References 26 publications

A leucine-to-proline mutation in the putative first transmembrane domain of the 22-kDa peripheral myelin protein in the trembler-J mouse.

A leucine-to-proline mutation in the putative first transmembrane domain of the 22-kDa peripheral myelin protein in the trembler-J mouse.

Pleiotropy in microdeletion syndromes: neurologic and spermatogenic abnormalities in mice homozygous for the p6H deletion are likely due to dysfunction of a single gene.

Effects of Gas1 on gliomas: a review on current preclinical studies

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