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No premature gene expression in germ cells of embryos deriving from nos females.


Heller, A; Steinmann-Zwicky, M (1998). No premature gene expression in germ cells of embryos deriving from nos females. Mechanisms of Development, 72(1-2):169-173.

Abstract

The product of nos is required at the posterior pole of the embryo for the differentiation of abdominal structures, but not for pole cell formation. A previous analysis that reported the expression of germline-specific enhancer-trap lines suggested that nos also controls the timing of the initiation of transcription of germline-specific genes. Here we repeat the experiments that led to this hypothesis and we report further experiments. Our results show that, contrary to what had been reported, germ cells of embryos deriving from nos females do not show premature gene expression. Germ cells of such embryos, however, often show artefactual lacZ staining even in the absence of a lacZ gene.

Abstract

The product of nos is required at the posterior pole of the embryo for the differentiation of abdominal structures, but not for pole cell formation. A previous analysis that reported the expression of germline-specific enhancer-trap lines suggested that nos also controls the timing of the initiation of transcription of germline-specific genes. Here we repeat the experiments that led to this hypothesis and we report further experiments. Our results show that, contrary to what had been reported, germ cells of embryos deriving from nos females do not show premature gene expression. Germ cells of such embryos, however, often show artefactual lacZ staining even in the absence of a lacZ gene.

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Additional indexing

Item Type:Journal Article, refereed
Communities & Collections:07 Faculty of Science > Institute of Molecular Life Sciences
Dewey Decimal Classification:570 Life sciences; biology
Scopus Subject Areas:Health Sciences > Embryology
Life Sciences > Developmental Biology
Language:English
Date:1 March 1998
Deposited On:11 Feb 2008 12:16
Last Modified:01 Dec 2023 02:38
Publisher:Elsevier
ISSN:0925-4773
OA Status:Closed
Publisher DOI:https://doi.org/10.1016/S0925-4773(98)00020-3
PubMed ID:9533961
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