scholarly journals Molecular genetic basis of flower colour variegation in Linaria

2007 ◽  
Vol 89 (3) ◽  
pp. 129-134 ◽  
Author(s):  
LISETE GALEGO ◽  
JORGE ALMEIDA
Keyword(s):  
Molecular Basis ◽  
Genetic Basis ◽  
Anthocyanin Biosynthesis ◽  
Molecular Genetic ◽  
Flower Colour ◽  
Close Relative ◽  
Model Species ◽  
Gene Encoding ◽  
Genetic Studies ◽  
Molecular Genetic Basis

SummaryTo identify transposons that may be of use for mutagenesis we investigated the genetic molecular basis of a case of flower colour variegation in Linaria, a close relative of the model species Antirrhinum majus. We show that this variegation is attributable to an unstable mutant allele of the gene encoding dihydroflavonol-4-reductase, one of the enzymes required for anthocyanin biosynthesis. This allele carries an insertion of a transposon belonging to the CACTA family (Tl1, Transposon Linaria 1) which blocks its expression thus conferring an ivory flower colour phenotype. Tl1 is occasionally excised in dividing epidermal cells to produce clonal patches of red tissue on the ivory background, and in cells giving rise to gametes to generate reversion alleles conferring a fully coloured phenotype. This finding may open the way for targeted transposon-mutagenesis in Linaria, and hence for using this genus in comparative genetic studies.

scholarly journals Molecular Basis of Rifampin and Isoniazid Resistance in Mycobacterium bovis Strains Isolated in Sardinia, Italy

2001 ◽  
Vol 45 (6) ◽  
pp. 1645-1648 ◽  
Author(s):  
L. A. Sechi ◽  
S. Zanetti ◽  
M. Sanguinetti ◽  
P. Molicotti ◽  
L. Romano ◽  
...  
Keyword(s):  
Mycobacterium Bovis ◽  
Molecular Basis ◽  
Genetic Basis ◽  
Molecular Genetic ◽  
Geographic Area ◽  
Frequent Mutation ◽  
Isoniazid Resistance ◽  
Molecular Genetic Basis ◽  
Sequence Variations ◽  
Rifampin Resistance

ABSTRACT Fourteen of 22 (68%) Mycobacterium bovis strains isolated from cattle in Sardinia were found to be resistant to rifampin and isoniazid. Analysis of the rpoB and the katG, oxyR-ahpC, and inhA gene regions of these strains was performed in order to investigate the molecular basis of rifampin and isoniazid resistance, respectively. The most frequent mutation, encountered in 6 of 10 strains (60%), was in the rpoBgene; it occurred, at codon position 521 and resulted in leucine changed to proline. This suggests that codon 521 may be important for the development of rifampin resistance in M. bovis. Resistance to isoniazid is associated in Mycobacterium tuberculosis with a variety of mutations affecting one or more genes. Our results confirm the difficulty of interpreting the sequence variations observed in clinical strains of M. bovis. M. bovis strains isolated from the same geographic area showed similar mutations within the genes responsible for rifampin and isoniazid resistance. Our results represent the first study to elucidate the molecular genetic basis of drug resistance in M. bovis isolated from cattle.

oPnosDsA ib F le m lo o c le a c ti uolnesdoefdCurcoemdefrrosm ys t M em AI EaAntt ig e e st nss Understanding of the biochemical structures and molecular basis of Rh antigens is emerging rapidly. Absence of Rh antigens, as occurs in the RhnuN phenotype, compromises the integrity of red cells and cells from people with an RhnuN phenotype have been extensively studied. These studies contributed to the recognition of Rh polypeptides and some related glycoproteins [see 20,21,22]. Partial amino acid sequencing of the proteins in Bristol, Paris and Baltimore [23,24,25] led to recognition of involvement of two genes and isolation of cDNA by the Paris and Bristol workers [26,27] and cloning of the D gene [28]. One gene is responsible for the D polypeptide and another for the C and E series of antigens. However, although encoded by the same gene there is evidence that the C and E series of antigens are carried by different proteins. The molecular genetic basis of Rh antigens is discussed in another presentation. Immune precipitation using anti-D, -c, -E or R6A antibodies demonstrated the proteins which carried the Rh antigens. Two bands are co-precipitated by anti-D: one with an apparent Mr 30,000 called D30 polypeptide by the Bristol group and the other a diffuse band of 50-100 kD called the D50 polypeptide. Similar bands were observed when immune precipitation were done using anti-c, -E or R6A [see 20-22]. The D30 polypeptide was an unusual membrane protein because it was not glycosylated, the gene producing this protein and the other Rh protein were subsequently cloned. Assignment of the genes to chromosome 1p34-p36 confirmed that they are responsible for the Rh polymorphism [see 22]. The role of the Rh glycoproteins, the diffuse band of 50-1 OOkD, is not yet understood: the gene encoding the Rh glycoprotein when cloned was assigned to chromosome 6p21-qter [29].

1995 ◽  
pp. 192-192
Keyword(s):  
Molecular Basis ◽  
Molecular Genetic ◽  
The Other ◽  
Diffuse Band ◽  
Gene Encoding ◽  
Molecular Genetic Basis ◽  
Immune Precipitation ◽  
Rh Glycoproteins ◽  
Chromosome 1P34

scholarly journals The Molecular-Genetic Basis of Functional Hyperandrogenism and the Polycystic Ovary Syndrome

2005 ◽  
Vol 26 (2) ◽  
pp. 251-282 ◽  
Author(s):  
Héctor F. Escobar-Morreale ◽  
Manuel Luque-Ramírez ◽  
José L. San Millán
Keyword(s):  
Environmental Factors ◽  
Polycystic Ovary Syndrome ◽  
Diagnostic Criteria ◽  
Genetic Basis ◽  
Polycystic Ovary ◽  
Molecular Genetic ◽  
Ovary Syndrome ◽  
The Metabolic Syndrome ◽  
Molecular Genetic Basis ◽  
Functional Hyperandrogenism

The genetic mechanisms underlying functional hyperandrogenism and the polycystic ovary syndrome (PCOS) remain largely unknown. Given the large number of genetic variants found in association with these disorders, the emerging picture is that of a complex multigenic trait in which environmental influences play an important role in the expression of the hyperandrogenic phenotype. Among others, genomic variants in genes related to the regulation of androgen biosynthesis and function, insulin resistance, and the metabolic syndrome, and proinflammatory genotypes may be involved in the genetic predisposition to functional hyperandrogenism and PCOS. The elucidation of the molecular genetic basis of these disorders has been burdened by the heterogeneity in the diagnostic criteria used to define PCOS, the limited sample size of the studies conducted to date, and the lack of precision in the identification of ethnic and environmental factors that trigger the development of hyperandrogenic disorders. Progress in this area requires adequately sized multicenter collaborative studies after standardization of the diagnostic criteria used to classify hyperandrogenic patients, in whom modifying environmental factors such as ethnicity, diet, and lifestyle are identified with precision. In addition to classic molecular genetic techniques such as linkage analysis in the form of a whole-genome scan and large case-control studies, promising genomic and proteomic approaches will be paramount to our understanding of the pathogenesis of functional hyperandrogenism and PCOS, allowing a more precise prevention, diagnosis, and treatment of these prevalent disorders.

scholarly journals A Molecular Genetic Basis Explaining Altered Bacterial Behavior in Space

PLoS ONE ◽  
2016 ◽  
Vol 11 (11) ◽  
pp. e0164359 ◽  
Author(s):  
Luis Zea ◽  
Nripesh Prasad ◽  
Shawn E. Levy ◽  
Louis Stodieck ◽  
Angela Jones ◽  
...  
Keyword(s):  
Genetic Basis ◽  
Molecular Genetic ◽  
Molecular Genetic Basis

Clinical and genetic parallels of the classification and diagnosis of Ehlers-Danlos syndrome

2021 ◽  
pp. 14-26
Author(s):  
Д.Д. Надыршина ◽  
А.В. Тюрин ◽  
Э.К. Хуснутдинова ◽  
Р.И. Хусаинова
Keyword(s):  
Genetic Counseling ◽  
Family Medicine ◽  
Genetic Basis ◽  
Molecular Genetic ◽  
Hereditary Disease ◽  
Orphan Diseases ◽  
Ehlers Danlos Syndrome ◽  
General Medical Practice ◽  
Molecular Genetic Basis ◽  
Danlos Syndrome

Статья посвящена обсуждению подходов к классификации и обзору доступных литературных данных о клинической вариабельности и молекулярно-генетических основах патогенеза редкого наследственного заболевания - синдрома Элерса-Данло. Представленный обзор расширит представление о патогенезе и позволит оптимизировать диагностику данного синдрома, определить тактику лечения и медико-генетического консультирования отягощенных семей как клиническим генетикам, специалистам в области изучения орфанных заболеваний, так и врачам терапевтам, специалистам семейной медицины и общей врачебной практики. The article is devoted to the discussion of approaches to the classification and review of the available literature data on clinical variability and the molecular genetic basis of the pathogenesis of a rare hereditary disease - Ehlers-Danlos syndrome. The presented review will expand the understanding of the pathogenesis and allow to optimize the diagnosis of this syndrome, to determine the tactics of treatment and medical and genetic counseling of burdened families, both to clinical geneticists, specialists in the study of orphan diseases, and to general practitioners, specialists in family medicine and general medical practice.

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