Expression-based assay of an X-linked gene to examine effects of the X-controlling element (Xce) locus

2000 ◽  
Vol 11 (5) ◽  
pp. 405-408 ◽  
Author(s):  
Robert M. Plenge ◽  
Ivona Percec ◽  
Joseph H. Nadeau ◽  
Huntington F. Willard
Development ◽  
1991 ◽  
Vol 111 (4) ◽  
pp. 1109-1120 ◽  
Author(s):  
D.D. Pravtcheva ◽  
C.N. Adra ◽  
F.H. Ruddle

In mouse development, the paternal allele of the X-linked gene Pgk-1 initiates expression on day 6, two days later than the maternal allele, which is activated on day 4. The different timing of expression of the maternal and paternal alleles may be determined by (i) imprinting of the chromosome region in which the gene resides, but not aimed specifically at the Pgk-1 gene; (ii) gene specific imprinting, acting on Pgk-1 irrespective of the chromosomal localization of the gene; (iii) an interplay between embryo cell differentiation, timing of X-inactivation and Pgk-1 expression, without the involvement of imprinting at the Pgk-1 locus itself (Fundele R., Illmensee, K., Jagerbauer, E. M., Fehlau, M. and Krietsch, W. K. (1987) Differentiation 35, 31–36). Our findings in transgenic mouse lines, carrying Pgk-1 on autosomes, indicate the importance of the X chromosomal location for the delayed expression of the paternal Pgk-1 allele, and are in agreement with the first of the explanations listed above. We propose that the late activation of the paternal Pgk-1 locus is a consequence of imprinting targeted at, and centered around, the X chromosome controlling element.


2000 ◽  
Vol 63 (2) ◽  
pp. 469-481 ◽  
Author(s):  
V. Anne Westbrook ◽  
Alan B. Diekman ◽  
Ken L. Klotz ◽  
Vrinda V. Khole ◽  
Chris von Kap-Herr ◽  
...  

1974 ◽  
Vol 23 (2) ◽  
pp. 175-184 ◽  
Author(s):  
Joseph Greenberg ◽  
Leonard J. Berends ◽  
John Donch ◽  
Michael H. L. Green

SUMMARYPAM 26, a radiation-sensitive mutant ofEscherichia colistrain B, is described. Its properties are attributable to a mutation in a gene,exrB, which is cotransducible withmalB. It differs fromuvrA(alsomalB-linked) derivatives of strain B in being sensitive to 1-methyl-3-nitro-1-nitroso-guanidine and γ-radiation, and in being able to reactivate UV-irradiated phage T3. It differs fromexrA(alsomalB-linked) derivatives of strain B in forming filaments during the course of normal growth as well as after irradiation. WhenexrBwas transduced into a K12 (lon+) strain, filaments did not form spontaneously. Three-point transductions established the order of markers asmet A malB exrB. Based on an analysis of the frequency of wild-type recombinants in a reciprocal transduction betweenexrAandexrBstrains, it was inferred that they are not isogenic and that the order of markers ismalB exrA exrB.


2021 ◽  
Author(s):  
A. L. Romero-Olivares ◽  
E. W. Morrison ◽  
A. Pringle ◽  
S. D. Frey

AbstractFungi are mediators of the nitrogen and carbon cycles in terrestrial ecosystems. Examining how nitrogen uptake and organic matter decomposition potential differs in fungi can provide insight into the underlying mechanisms driving fungal ecological processes and ecosystem functioning. In this study, we assessed the frequency of genes encoding for specific enzymes that facilitate nitrogen uptake and organic matter decomposition in 879 fungal genomes with fungal taxa grouped into trait-based categories. Our linked gene-trait data approach revealed that gene frequencies vary across and within trait-based groups and that trait-based categories differ in trait space. We present two examples of how this linked gene-trait approach can be used to address ecological questions. First, we show that this type of approach can help us better understand, and potentially predict, how fungi will respond to environmental stress. Specifically, we found that trait-based categories with high nitrogen uptake gene frequency increased in relative abundance when exposed to high soil nitrogen enrichment. Second, by comparing frequencies of nitrogen uptake and organic matter decomposition genes, we found that most ectomycorrhizal fungi in our dataset have similar gene frequencies to brown rot fungi. This demonstrates that gene-trait data approaches can shed light on potential evolutionary trajectories of life history traits in fungi. We present a framework for exploring nitrogen uptake and organic matter decomposition gene frequencies in fungal trait-based groups and provide two concise examples on how to use our framework to address ecological questions from a mechanistic perspective.


1985 ◽  
Vol 5 (10) ◽  
pp. 2677-2683
Author(s):  
J M Boss ◽  
R Mengler ◽  
K Okada ◽  
C Auffray ◽  
J L Strominger

The DP subregion of the human major histocompatibility complex contains two closely linked gene pairs, DP alpha, DP beta and SX alpha, SX beta. The exon-intron organization and the complete DNA sequence of the SX alpha gene are reported here. There are several mutations within the SX alpha gene which strongly suggest that it is a pseudogene. These include two frameshift mutations, one in the alpha 1 domain and the other in the cytoplasmic domain. A 5' splice site mutation at the end of the alpha 1 exon also exists. DNA sequence homology between DP alpha and SX alpha suggests that these genes arose through a gene duplication event.


1982 ◽  
Vol 40 (2) ◽  
pp. 139-147 ◽  
Author(s):  
Sohaila Rastan

SUMMARYPrevious studies have shown that different alleles of the mouse X chromosomal controlling element locus, Xce, cause non-random X-chromosome inactivation as judged by variegation in the coats of female mice heterozygous for X-linked coat colour/structure genes, or Cattanach's translocation (Is (X; 7) Ct), or the relative activity of biochemical variants of the X-linked enzyme PGK. This paper presents evidence using the Kanda differential staining method on 6½ d.p.c. and 13½ d.p.c. female mouse embryos heterozygous for the marker X chromosome Is (X; 7) Ct and carrying different Xce alleles, that the Xce locus affects the randomness of X chromosome inactivation. Furthermore the fact that a marked Xce effect is demonstrable in female embryos as early as 6½ d.p.c. (i.e. very soon after the initial time of X-inactivation) is strong evidence that the Xce locus exerts its effect by causing primary non-random X-inactivation rather than by cell selection after initial random X-inactivation.


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