Restoration of the Mendelian transmission ratio by a deletion in the mouse chromosome 1 HSR

Dieter Weichenhan; Bärbel Kunze; Walther Traut; Heinz Winking

doi:10.1017/S0016672398003206

Restoration of the Mendelian transmission ratio by a deletion in the mouse chromosome 1 HSR

Dieter Weichenhan^*, Bärbel Kunze, Walther Traut, Heinz Winking

^*Corresponding author for this work

Institute of Biology

7 Citations (Scopus)

Abstract

The house mouse, Mus musculus, harbours a variable cluster of long-range repeats in chromosome 1. As shown in previous studies, some high-copy clusters such as the MUT cluster are cytogenetically apparent as a homogeneously staining region (HSR) and are associated with a distortion of the Mendelian recovery ratio when transmitted by heterozygous females. The effect is caused by a decreased viability of +/+ embryos. It is compensated by maternal or paternal MUT. In this study, a deletion derivative of MUT, MUT(del), shows normal transmission ratios and no compensating capability. In this respect, MUT(del) behaves like a wild-type cluster. Hence, both properties - transmission ratio distortion and compensating capability - map to the deleted region. The deletion comprises three-quarters of the MUT HSR and does not extend to the nearest markers adjacent to the HSR.

Original language	English
Journal	Genetical Research
Volume	71
Issue number	2
Pages (from-to)	119-125
Number of pages	7
ISSN	0016-6723
DOIs	https://doi.org/10.1017/S0016672398003206
Publication status	Published - 04.1998

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Academic Focus: Center for Infection and Inflammation Research (ZIEL)

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10.1017/S0016672398003206

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title = "Restoration of the Mendelian transmission ratio by a deletion in the mouse chromosome 1 HSR",

abstract = "The house mouse, Mus musculus, harbours a variable cluster of long-range repeats in chromosome 1. As shown in previous studies, some high-copy clusters such as the MUT cluster are cytogenetically apparent as a homogeneously staining region (HSR) and are associated with a distortion of the Mendelian recovery ratio when transmitted by heterozygous females. The effect is caused by a decreased viability of +/+ embryos. It is compensated by maternal or paternal MUT. In this study, a deletion derivative of MUT, MUT(del), shows normal transmission ratios and no compensating capability. In this respect, MUT(del) behaves like a wild-type cluster. Hence, both properties - transmission ratio distortion and compensating capability - map to the deleted region. The deletion comprises three-quarters of the MUT HSR and does not extend to the nearest markers adjacent to the HSR.",

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T1 - Restoration of the Mendelian transmission ratio by a deletion in the mouse chromosome 1 HSR

AU - Weichenhan, Dieter

AU - Kunze, Bärbel

AU - Traut, Walther

AU - Winking, Heinz

PY - 1998/4

Y1 - 1998/4

N2 - The house mouse, Mus musculus, harbours a variable cluster of long-range repeats in chromosome 1. As shown in previous studies, some high-copy clusters such as the MUT cluster are cytogenetically apparent as a homogeneously staining region (HSR) and are associated with a distortion of the Mendelian recovery ratio when transmitted by heterozygous females. The effect is caused by a decreased viability of +/+ embryos. It is compensated by maternal or paternal MUT. In this study, a deletion derivative of MUT, MUT(del), shows normal transmission ratios and no compensating capability. In this respect, MUT(del) behaves like a wild-type cluster. Hence, both properties - transmission ratio distortion and compensating capability - map to the deleted region. The deletion comprises three-quarters of the MUT HSR and does not extend to the nearest markers adjacent to the HSR.

AB - The house mouse, Mus musculus, harbours a variable cluster of long-range repeats in chromosome 1. As shown in previous studies, some high-copy clusters such as the MUT cluster are cytogenetically apparent as a homogeneously staining region (HSR) and are associated with a distortion of the Mendelian recovery ratio when transmitted by heterozygous females. The effect is caused by a decreased viability of +/+ embryos. It is compensated by maternal or paternal MUT. In this study, a deletion derivative of MUT, MUT(del), shows normal transmission ratios and no compensating capability. In this respect, MUT(del) behaves like a wild-type cluster. Hence, both properties - transmission ratio distortion and compensating capability - map to the deleted region. The deletion comprises three-quarters of the MUT HSR and does not extend to the nearest markers adjacent to the HSR.

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Restoration of the Mendelian transmission ratio by a deletion in the mouse chromosome 1 HSR

Abstract

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