scholarly journals Molecular-genetic bases of plumage coloring in chicken

2019 ◽  
Vol 23 (3) ◽  
pp. 343-354
Author(s):  
A. V. Makarova ◽  
O. V. Mitrofanova ◽  
A. B. Vakhrameev ◽  
N. V. Dementeva
Keyword(s):  
Single Gene ◽  
Molecular Genetic ◽  
Receptor Activation ◽  
Structural Colors ◽  
Tyrosinase Gene ◽  
Key Factor ◽  
Mechanisms Of Formation ◽  
Genetic Mechanisms ◽  
Melanin Coloration ◽  
Breeding Groups

The color of plumage in birds is an important feature, often determining descent to a particular species or breed. It serves as a key factor in the interaction of birds with each other due to their well-developed visual perception of the surrounding world. In poultry including chickens, the color of the plumage can be treated as a genetic marker, useful for identifying breeds, populations and breeding groups with their specific traits. The origin of diverse color plumage is the result of two interrelated physical processes, chemical and optical, due to which pigment and structural colors in the color are formed. The pigment melanin, which is presented in two forms, eumelanin and pheomelanin, is widely spread in birds. The basis for the formation of melanin is the aromatic amino acid tyrosine. The process of melano-genesis involves many loci, part of the complex expression of plumage color genes. In birds, the solid black color locus encodes the melanocortin 1 receptor (MC1R), mutations in which lead to a change in receptor activation and form different variants of the E locus. Using the GWAS analysis, possible genes affecting the formation of color in chickens were detected. The biosynthesis and types of melanin are affected by the activity of the enzyme tyrosine, and mutations in the tyrosinase gene (TYR) cause albinism in different species. The formation mechanism of brown, silver, gold, lavender and a number of other shades is determined by the influence on the work of the MC1R genes and TYR specific modifier genes. Thus, locus I currently associated with the PMEL17 gene inhibits the expression of eumelanin, and the MLPH gene affects tyrosinase function. Research on the mechanisms of formation of the secondary coloring of plumage in chickens is being actively conducted nowadays. The formation of a marble feather pattern is associated with the mutation of the endothelin B2 receptor (EDNRB2), in the coding part of the gene of which a polymorphism is found associated with the mo locus. The molecular base that causes the feather banding (locus B and autosomal recessive banding) is identified. Today, only some genes that determine the color of the plumage of chickens are studied and described. Different genes can produce similar plumage patterns, and different phenotypes can be determined by the polymorphism of a single gene. Using molecular methods, you can more accurately identify these differences. This overview shows the nature of melanin coloration in birds using the example of chickens of various breeds and also attempts to systematize knowledge about the molecular-genetic mechanisms of the appearance of various types of coloration.

The formation mechanisms of tumor-associated tissue eosinophilia in gastric cancer and colon cancer

2017 ◽  
pp. 74-80
Author(s):  
В.В. Новицкий ◽  
К.И. Янкович ◽  
Ю.В. Колобовникова ◽  
А.И. Дмитриева ◽  
О.И. Уразова ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Colon Cancer ◽  
Tumor Tissue ◽  
Molecular Genetic ◽  
Formation Mechanisms ◽  
Tissue Samples ◽  
Tissue Eosinophilia ◽  
Neoplastic Lesion ◽  
Key Factor ◽  
Mechanisms Of Formation

Опухолеассоциированная тканевая эозинофилия определяется как эозинофильная инфильтрация стромы опухоли. Эта реакция, как полагают, играет важную роль в канцерогенезе. Считается, что эозинофилы обладают противоопухолевой активностью за счет высвобождения цитотоксических белков. Цель исследования - изучение молекулярно-генетических механизмов формирования опухолеассоциированной тканевой эозинофилии у больных раком желудка и толстой кишки. Методика. Материалом исследования служили образцы опухолевой ткани пациентов с диагнозом рак желудка или толстой кишки . Подсчитывали количество эозинофилов, инфильтрирующих опухолевую ткань, а также оценивали экспрессию эотаксина-1 (ключевого фактора хемотаксиса эозинофилов) и его рецептора CCR3 в опухолевой ткани методом иммуногистохимии. Было изучено распределение полиморфных вариантов генов CCL11 (А384G) , CCR3 (T51С) , IL5 (С703Т) и IL5R (G80А) . Геномную ДНК выделяли из образцов опухолевой ткани. Генотипирование образцов ДНК по полиморфизмам генов осуществляли путем ПДРФ-анализа продуктов ПЦР-амплификации специфических участков генома с последующей визуализацией в ультрафиолетовом свете. Результаты. Показана более высокая экспрессия эотаксина-1 и CCR3 в ткани опухоли при раке желудка и толстой кишки, ассоциированном с эозинофилией. Установлена ассоциация эозинофильной инфильтрации опухолевой ткани с носительством генотипа СС и аллеля С полиморфизма T51С гена CCR3 и генотипа СС и аллеля С полиморфизма С703Т гена IL5 . Заключение. Формирование опухолеассоциированной тканевой эозинофилии при раке желудка и толстой кишки опосредованно действием эотаксина-1 и его рецептора. Результаты молекулярно-генетического исследования указывают на генетически детерминированный характер эозинофилии при раке желудка и толстой кишки. Tumor-associated tissue eosinophilia is defined as eosinophilic stromal infiltration of a tumor. Tumor-associated tissue eosinophilia is believed to play a significant role in carcinogenesis. It is believed that eosinophils have antitumor activity due to the release of cytotoxic proteins. The aim of this study was to investigate the molecular-genetic mechanisms of formation of tumor-associated tissue eosinophilia in patients with gastric cancer and colon cancer. Methods. Tumor tissue samples from patients with gastric cancer and colon cancer were reviewed. We counted the number of infiltrating eosinophils in neoplastic lesion tissue and we evaluated the expression of eotaxin-1 (a key factor of chemotaxis of eosinophils) and its receptor CCR3 in tumor tissue by immunohistochemical staining. The distribution of polymorphic variants of genes CCL11 (А384G), CCR3 (Т51С), IL5 (С703Т) and of the IL5R (G80А) was studied. DNA was isolated from tumor tissue samples. Genotyping of polymorphisms was carried out by polymerase chain reaction (PCR), followed by digestion with the appropriate restriction enzyme (PCR-RFLP) and agarose-gel electrophoresis. Results. It is shown that higher expression eotaxin-1 and CCR3 is determined in the tumor tissue of gastric cancer and colon cancer associated with eosinophilia. It is established that eosinophilic infiltration of the tumor tissue is associated with the carriers of CC genotype and C allele of the gene CCR3 (Т51С) and CC genotype and C allele of gene IL5 (С703Т) . Conclusion. The formation of tumor-associated tissue eosinophilia in gastric cancer and colon cancer is mediated through the action eotaxin-1 and its receptor. The results of molecular-genetic studies indicate a genetically determined character of eosinophilia in gastric cancer and colon cancer.

Can Autoimmune Mechanisms Account for the Genetic Predisposition to Schizophrenia?

1992 ◽  
Vol 160 (4) ◽  
pp. 533-540 ◽  
Author(s):  
John Knight ◽  
Allison Knight ◽  
Gabor Ungvari
Keyword(s):  
Genetic Predisposition ◽  
Single Gene ◽  
Molecular Genetic ◽  
Genetic Mechanism ◽  
Single Gene Disorders ◽  
Genetic Mechanisms ◽  
Genetic Techniques

Applications of molecular genetic techniques to schizophrenia have shown great initial promise but have then proved disappointing. In order to maximise chances of elucidating the genetic mechanism underlying schizophrenia, diverse strategies and diverse perspectives must be adopted. Most studies begin with the premise that, although schizophrenia may be a heterogeneous collection of diseases, some subtypes will be primarily single-gene disorders. We are concerned that this single-gene hypothesis may be incorrect. Schizophrenia research may benefit from application of knowledge from other disciplines and from other diseases which, in terms of epidemiology and apparent genetic mechanisms, bear some resemblance to schizophrenia.

scholarly journals Molecular genetics of bipolar disorder

2001 ◽  
Vol 178 (S41) ◽  
pp. s128-s133 ◽  
Author(s):  
Nick Craddock ◽  
Ian Jones
Keyword(s):  
Bipolar Disorder ◽  
Candidate Gene ◽  
Molecular Genetics ◽  
Ethical Issues ◽  
Association Studies ◽  
Single Gene ◽  
Molecular Genetic ◽  
Genetic Dissection ◽  
Adoption Studies ◽  
Candidate Gene Association

BackgroundA robust body of evidence from family, twin and adoption studies demonstrates the importance of genes in the pathogenesis of bipolar disorder. Recent advances in molecular genetics have made it possible to identify these susceptibility genes.AimsTo present an overview for clinical psychiatrists.MethodReview of current molecular genetics approaches and emerging findings.ResultsOccasional families may exist in which a single gene plays a major role in determining susceptibility, but the majority of bipolar disorder involves more complex genetic mechanisms such as the interaction of multiple genes and environmental factors. Molecular genetic positional and candidate gene approaches are being used for the genetic dissection of bipolar disorder. No gene has yet been identified but promising findings are emerging. Regions of interest include chromosomes 4p16, 12q23–q24, 16p13, 21q22, and Xq24–q26. Candidate gene association studies are in progress but no robust positive findings have yet emerged.ConclusionIt is almost certain that over the next few years the identification of bipolar susceptiblity genes will have a major impact on our understanding of disease pathophysiology. This is likely to lead to major improvements and treatment in patient care, but will also raise important ethical issues.

Epigenetics and Applied Anthropology

2021 ◽  
Author(s):  
Charles H. Klein
Keyword(s):  
Social Inequalities ◽  
Homo Sapiens ◽  
Single Gene ◽  
Molecular Genetic ◽  
Healthcare Providers ◽  
Basic Research ◽  
Sufficient Information ◽  
Theoretical Frameworks ◽  
Noncoding Dna ◽  
Wide Range

Since Francis Crick and James D. Watson’s discovery of DNA in 1953, researchers, policymakers, and the general public have sought to understand the ways in which genetics shapes human lives. A milestone in these efforts was the completion of the Human Genome Project’s (HGP) sequencing of Homo sapiens’ nearly three million base pairs in 2003. Yet, despite the excitement surrounding the HGP and the discovery of the structural genetic underpinnings of several debilitating diseases, the vast majority of human health outcomes have not been linked to a single gene. Moreover, even when genes have been associated with particular diseases (e.g., breast and colon cancer), it is not well understood why certain genetically predisposed individuals become ill and others do not. Nor has the HGP’s map provided sufficient information to understand the actual functioning of the human genetic code, including the role of noncoding DNA (“junk DNA”) in regulating molecular genetic processes. In response, a growing number of scientists have shifted their attention from structural genetics to epigenetics, the study of how genes express themselves in particular situations and environments. Anthropologists play roles in these applications of epigenetics to real-world settings. Their new theoretical frameworks unsettle the nature-versus-nurture binary and support biocultural anthropological research demonstrating how race becomes biology and embodies social inequalities and health disparities across generations. Ethnographically grounded case studies further highlight the diverse epigenetic logics held by healthcare providers, researchers, and patient communities and how these translations of scientific knowledge shape medical practice and basic research. The growing field of environmental epigenetics also offers a wide range of options for students and practitioners interested in applying the anthropological toolkit in epigenetics-related work.

scholarly journals Isoprocurcumenol Supports Keratinocyte Growth and Survival through Epidermal Growth Factor Receptor Activation

2021 ◽  
Vol 22 (22) ◽  
pp. 12579
Author(s):  
Paul Kwangho Kwon ◽  
Sung Wook Kim ◽  
Ranjit De ◽  
Sung Woo Jeong ◽  
Kyong-Tai Kim
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Receptor Activation ◽  
Cellular Damage ◽  
Major Type ◽  
Growth And Survival ◽  
Biosensor System ◽  
Key Factor ◽  
Epidermal Growth

Although proliferation of keratinocytes, a major type of skin cells, is a key factor in maintaining the function of skin, their ability to proliferate tends to diminish with age. To solve such a problem, researchers in medical and skin cosmetic fields have tried to utilize epidermal growth factor (EGF), but achieved limited success. Therefore, a small natural compound that can mimic the activity of EGF is highly desired in both medical and cosmetic fields. Here, using the modified biosensor system, we observed that natural small-compound isoprocurcumenol, which is a terpenoid molecule derived from turmeric, can activate EGFR signaling. It increased the phosphorylation of ERK and AKT, and upregulated the expression of genes related to cell growth and proliferation, such as c-myc, c-jun, c-fos, and egr-1. In addition, isoprocurcumenol induced the proliferation of keratinocytes in both physical and UVB-induced cellular damage, indicative of its function in skin regeneration. These findings reveal that EGF-like isoprocurcumenol promotes the proliferation of keratinocytes and further suggest its potential as an ingredient for medical and cosmetics use.

scholarly journals Comparative transcriptome analysis of mule uncovered several heterosis-related genes for improving muscular endurance and cognition

2019 ◽  
Author(s):  
Shan Gao
Keyword(s):  
Alternative Splicing ◽  
Molecular Genetic ◽  
Hybrid Vigor ◽  
Neuronal System ◽  
Future Studies ◽  
Genome Wide ◽  
A Genome ◽  
Genetic Mechanisms ◽  
Productive Traits ◽  
Genome Wide Gene Expression

AbstractHeterosis has been widely exploited in animal and plant breeding to enhance the productive traits of hybrid progeny of two breeds or two species. Although, there were multiple models for explaining the hybrid vigor, such as dominance and over-dominance hypothesis, its underlying molecular genetic mechanisms remain equivocal. The aim of this study is through comparing the different expression genes (DEGs) and different alternative splicing (DAS) genes to explore the mechanism of heterosis. Here, we performed a genome-wide gene expression and alternative splicing analysis of two heterotic crosses between donkey and horse in three tissues. The results showed that the DAS genes influenced the heterosis-related phenotypes in a unique than DEGs and about 10% DEGs are DAS genes. In addition, over 69.7% DEGs and 87.2% DAS genes showed over-dominance or dominance, respectively. Furthermore, the “Muscle Contraction” and “Neuronal System” pathways were significantly enriched both for the DEGs and DAS genes in muscle. TNNC2 and RYR1 genes may contribute to mule’s great endurance while GRIA2 and GRIN1 genes may be related with mule’s cognition. Together, these DEGs and DAS genes provide the candidates for future studies of the genetic and molecular mechanism of heterosis in mule.

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