Constitutive Mutation

A HISTIDINE OPERATOR-CONSTITUTIVE MUTATION DECREASES THE FREQUENCY OF RECOMBINATION WITHIN THE HISTIDINE OPERON OF SALMONELLA TYPHIMURIUM

Genetics ◽

10.1093/genetics/71.3.461 ◽

1972 ◽

Vol 71 (3) ◽

pp. 461-464

Author(s):

Dragutin J Savic

Keyword(s):

Salmonella Typhimurium ◽

Gene Region ◽

Constitutive Mutation

Abstract A constitutive mutation in the histidine operon in Salmonella leads to a decrease in the recombinant recovery following transduction with P22 phage. This decrease appears to be a true decrease in recombination within the histidine operon and specific to that gene region. In addition, a strain with an unlinked mutation was isolated in which an operator-constitutive mutation is lethal.

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Mutations Causing Constitutive Invertase Synthesis in Yeast: Genetic Interactions with snf Mutations

Genetics ◽

10.1093/genetics/115.2.247 ◽

1987 ◽

Vol 115 (2) ◽

pp. 247-253

Author(s):

Lenore Neigeborn ◽

Marian Carlson

Keyword(s):

Regulatory Region ◽

Constitutive Expression ◽

Genetic Interactions ◽

The Third ◽

Recessive Mutations ◽

Constitutive Mutation ◽

Complementation Groups ◽

High Level ◽

Yeast Genetic ◽

Very High

ABSTRACT We have selected 210 mutants able to grow on sucrose in the presence of 2-deoxyglucose. We identified recessive mutations in three major complementation groups that cause constitutive (glucose-insensitive) secreted invertase synthesis. Two groups comprise alleles of the previously identified HXK2 and REG1 genes, and the third group was designated cid1 (constitutive invertase derepression). The effect of cid1 on SUC2 expression is mediated by the SUC2 upstream regulatory region, as judged by the constitutive expression of a SUC2-LEU2-lacZ fusion in which the LEU2 promoter is under control of SUC2 upstream sequences. A cid1 mutation also causes glucose-insensitive expression of maltase. The previously isolated constitutive mutation ssn6 is epistatic to cid1, reg1 and hxk2 for very high level constitutive invertase expression. Mutations in SNF genes that prevent derepression of invertase are epistatic to cid1, reg1 and hxk2; we have previously shown that ssn6 has different epistasis relationships with snf mutations. The constitutive mutation tup1 was found to resemble ssn6 in its genetic interactions with snf mutations. These findings suggest that CID1, REG1 and HXK2 are functionally distinct from SSN6 and TUP1.

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Salmonella stimulate macrophage macropinocytosis and persist within spacious phagosomes.

Journal of Experimental Medicine ◽

10.1084/jem.179.2.601 ◽

1994 ◽

Vol 179 (2) ◽

pp. 601-608 ◽

Cited By ~ 215

Author(s):

C M Alpuche-Aranda ◽

E L Racoosin ◽

J A Swanson ◽

S I Miller

Keyword(s):

Bone Marrow ◽

Plasma Membrane ◽

Time Lapse ◽

Membrane Ruffling ◽

Mouse Macrophages ◽

Constitutive Mutation ◽

Microscopic Studies ◽

Specific Igg ◽

Salmonella Survival ◽

Time Lapse Video

Light microscopic studies of phagocytosis showed that Salmonella typhimurium entered mouse macrophages enclosed in spacious phagosomes (SP). Viewed by time-lapse video microscopy, bone marrow-derived macrophages exposed to S. typhimurium displayed generalized plasma membrane ruffling and macropinocytosis. Phagosomes containing Salmonella were morphologically indistinguishable from macropinosomes. SP formation was observed after several methods of bacterial opsonization, although bacteria opsonized with specific IgG appeared initially in small phagosomes that later enlarged. In contrast to macropinosomes induced by growth factors, which shrink completely within 15 min, SP persisted in the cytoplasm, enlarging often by fusion with macropinosomes or other SP. A Salmonella strain containing a constitutive mutation in the phoP virulence regulatory locus (PhoPc) induced significantly fewer SP. Similar to Yersinia enterocolitica, PhoPc bacteria entered macrophages in close-fitting phagosomes, consistent with that expected for conventional receptor-mediated phagocytosis. These results suggest that formation of SP contributes to Salmonella survival and virulence.

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A regulatory region responsible for proline-specific induction of the yeast PUT2 gene is adjacent to its TATA box.

Molecular and Cellular Biology ◽

10.1128/mcb.8.11.4634 ◽

1988 ◽

Vol 8 (11) ◽

pp. 4634-4641 ◽

Cited By ~ 15

Author(s):

A H Siddiqui ◽

M C Brandriss

Keyword(s):

Gene Fusion ◽

Regulatory Gene ◽

Regulatory Region ◽

Tata Box ◽

Homologous Gene ◽

Lacz Gene ◽

Proline Utilization ◽

Constitutive Mutation ◽

Necessary And Sufficient ◽

Utilization Pathway

Deletion analysis of the promoter of the PUT2 gene that functions in the proline utilization pathway of Saccharomyces cerevisiae identified a PUT2 upstream activation site (UAS). It is contained within a single 40-base-pair (bp) region located immediately upstream of the TATA box and is both necessary and sufficient for proline induction. When placed upstream of a CYC7-lacZ gene fusion, the 40-bp sequence conferred proline regulation on CYC7-lacZ. A 35-bp deletion within the PUT2 UAS in an otherwise intact PUT2 promoter resulted in noninducible expression of a PUT2-lacZ gene fusion. When a plasmid bearing this UAS-deleted promoter was placed in a strain carrying a constitutive mutation in the positive regulatory gene PUT3, expression of PUT2-lacZ was not constitutive but occurred at levels below those found under noninducing conditions. In heterologous as well as homologous gene fusions, the PUT2 UAS appeared to be responsible for uninduced as well as proline-induced levels of expression. Although located immediately adjacent to the PUT2 UAS, the TATA box did not appear to play a regulatory role, as indicated by the results of experiments in which it was replaced by the CYC7 TATA box. A 26-bp sequence containing this TATA box was critical to the expression of PUT2, since a deletion of this region completely abolished transcriptional activity of the gene under both inducing and noninducing conditions. Our results indicate that the PUT2 promoter has a comparatively simple structure, requiring UAS and TATA sequences as well as the PUT3 gene product (directly or indirectly) for its expression.

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Cyan Fluorescent Protein Carries a Constitutive Mutation That Prevents Its Dimerization

Biochemistry ◽

10.1021/bi1015875 ◽

2011 ◽

Vol 50 (4) ◽

pp. 437-439 ◽

Cited By ~ 20

Author(s):

Agathe Espagne ◽

Marie Erard ◽

Karine Madiona ◽

Valérie Derrien ◽

Gabriella Jonasson ◽

...

Keyword(s):

Fluorescent Protein ◽

Cyan Fluorescent Protein ◽

Constitutive Mutation

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TWO CLOSELY LINKED MUTATIONS IN DROSOPHILA MELANOGASTER THAT ARE LETHAL TO OPPOSITE SEXES AND INTERACT WITH DAUGHTERLESS

Genetics ◽

10.1093/genetics/90.4.683 ◽

1978 ◽

Vol 90 (4) ◽

pp. 683-697

Author(s):

Thomas W Cline

Keyword(s):

Maternal Effect ◽

Spontaneous Mutation ◽

Dominant Male ◽

Lethal Effects ◽

Male Specific Lethal ◽

Constitutive Mutation ◽

Sex Lethal ◽

The Right ◽

Female Specific ◽

Male Specific

ABSTRACT A new spontaneous mutation named Sex-lethal, Male-specific #1 (SxlM1) is described that is lethal to males, even in the presence of an Sxl + duplication. Females homozygous for SxlM1 are fully viable. This dominant, male-specific lethal mutation is on the X chromosome approximately 0.007 map units to the right of a previously isolated female-specific mutation, Female-lethal, here renamed Sex-lethal, Female-specific #1 (SxlF1). SxlM1 and SxlF1 are opposite in nearly every respect, particularly with regard to their interaction with the maternal effect of the autosomal mutation, daughterless (da). Females that are homozygous for da produce defective eggs that cannot support female (XX) development. A single dose of SxlM1 enables daughters to survive this da female-specific lethal maternal effect. A duplication of the Sxl locus weakly mimics this action of SxlM1. In contrast, SxlF1 and a deficiency for Sxl, strongly enhance the female-lethal effects of da. The actions of SxlM1 and SxlF1 are explained by a model in which expression of the Sxl locus is essential for females, lethal for males, and under the control of a product of the da locus. It is suggested that SxlM1 is a constitutive mutation at the Sxl locus.

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