scholarly journals Genetic Changes to a Transcriptional Silencer Element Confers Phenotypic Diversity within and between Drosophila Species

PLoS Genetics ◽  
2015 ◽  
Vol 11 (6) ◽  
pp. e1005279 ◽  
Author(s):  
Winslow C. Johnson ◽  
Alison J. Ordway ◽  
Masayoshi Watada ◽  
Jonathan N. Pruitt ◽  
Thomas M. Williams ◽  
...  
2019 ◽  
Vol 12 (4) ◽  
pp. 145-151 ◽  
Author(s):  
Andrzej Kowalski

The genetic changes accompanying a relocation of population to the captivity are mostly adverse and usually associated with deterioration of its status. These alterations are greater in small populations in which a loss of genetic variation limits the capability to adaptation. In this work, a status of small-sized guinea fowl and pheasant population relocated to the breeding is presented. These populations were analyzed based on the polymorphism of histone H1.c’, the protein for the first time identified as a heterogeneous. Histone H1.c’ was resolved in the two-dimensional polyacrylamide gel into the isoform H1.c’1 and H1.c’2, so its heterogeneity corresponds to the presence of homozygous phenotypes c’1 and c’2. Because no histone H1.c’ heterozygous phenotype was found, a significant phenotypic diversity in the guinea fowl ( P = 0.023) and pheasant ( P = 0.018) population was detected, together with its departures from Hardy-Weinberg equilibrium ( P < 0.0001). Both populations characterize an extreme loss of genetic diversity due to complete inbreeding ( F = 1) and an impact of genetic drift which, according to the expected values for guinea fowl (0.192) and pheasant (0.182) population, may strongly diminish allele frequency in the following generations. Thus, condition of populations evaluated based on the histone H1.c’ polymorphic variants, recognized as reasonable informative genetic markers (polymorphism information content of guinea fowl = 0.4 and pheasant = 0.38), corresponds to reduction of genetic variability caused by inbreeding and genetic drift. Therefore, it seems that rearing in the captivity can bring negative effects that favor restriction of animals’ vitality and survival of the population.


2018 ◽  
Author(s):  
Y. Czorlich ◽  
T. Aykanat ◽  
J. Erkinaro ◽  
P. Orell ◽  
CR. Primmer

AbstractUnderstanding the mechanisms by which populations adapt to their environments is a fundamental aim in biology. However, it remains challenging to identify the genetic basis of traits, provide evidence of genetic changes and quantify phenotypic responses. Age at maturity in Atlantic salmon represents an ideal trait to study contemporary adaptive evolution as it has been associated with a single locus in the vgll3 region, and has also strongly changed in recent decades. Here, we provide an empirical example of contemporary adaptive evolution of a large effect locus driving contrasting sex-specific evolutionary responses at the phenotypic level. We identified an 18% decrease in the vgll3 allele associated with late maturity (L) in a large and diverse salmon population over 36 years, induced by sex-specific selection during the sea migration. Those genetic changes resulted in a significant evolutionary response in males only, due to sex-specific dominance patterns and vgll3 allelic effects. The vgll3 allelic and dominance effects differed greatly in a second population and were likely to generate different selection and evolutionary patterns. Our study highlights the importance of knowledge of genetic architecture to better understand fitness trait evolution and phenotypic diversity. It also emphasizes the potential role of adaptive evolution in the trend toward earlier maturation observed in numerous Atlantic salmon populations worldwide.


2015 ◽  
Vol 112 (20) ◽  
pp. 6431-6436 ◽  
Author(s):  
Anthony R. Flores ◽  
Jessica Galloway-Peña ◽  
Pranoti Sahasrabhojane ◽  
Miguel Saldaña ◽  
Hui Yao ◽  
...  

The molecular mechanisms underlying pathogen emergence in humans is a critical but poorly understood area of microbiologic investigation. Serotype V group BStreptococcus(GBS) was first isolated from humans in 1975, and rates of invasive serotype V GBS disease significantly increased starting in the early 1990s. We found that 210 of 229 serotype V GBS strains (92%) isolated from the bloodstream of nonpregnant adults in the United States and Canada between 1992 and 2013 were multilocus sequence type (ST) 1. Elucidation of the complete genome of a 1992 ST-1 strain revealed that this strain had the highest homology with a GBS strain causing cow mastitis and that the 1992 ST-1 strain differed from serotype V strains isolated in the late 1970s by acquisition of cell surface proteins and antimicrobial resistance determinants. Whole-genome comparison of 202 invasive ST-1 strains detected significant recombination in only eight strains. The remaining 194 strains differed by an average of 97 SNPs. Phylogenetic analysis revealed a temporally dependent mode of genetic diversification consistent with the emergence in the 1990s of ST-1 GBS as major agents of human disease. Thirty-one loci were identified as being under positive selective pressure, and mutations at loci encoding polysaccharide capsule production proteins, regulators of pilus expression, and two-component gene regulatory systems were shown to affect the bacterial phenotype. These data reveal that phenotypic diversity among ST-1 GBS is mainly driven by small genetic changes rather than extensive recombination, thereby extending knowledge into how pathogens adapt to humans.


PLoS ONE ◽  
2010 ◽  
Vol 5 (5) ◽  
pp. e10485 ◽  
Author(s):  
Rui Sousa-Neves ◽  
Alexandre Rosas

Genes ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 101 ◽  
Author(s):  
Himeshi Samarasinghe ◽  
Man You ◽  
Thomas S. Jenkinson ◽  
Jianping Xu ◽  
Timothy Y. James

Hybridization is increasingly recognized as an important force impacting adaptation and evolution in many lineages of fungi. During hybridization, divergent genomes and alleles are brought together into the same cell, potentiating adaptation by increasing genomic plasticity. Here, we review hybridization in fungi by focusing on two fungal pathogens of animals. Hybridization is common between the basidiomycete yeast species Cryptococcus neoformans × Cryptococcus deneoformans, and hybrid genotypes are frequently found in both environmental and clinical settings. The two species show 10–15% nucleotide divergence at the genome level, and their hybrids are highly heterozygous. Though largely sterile and unable to mate, these hybrids can propagate asexually and generate diverse genotypes by nondisjunction, aberrant meiosis, mitotic recombination, and gene conversion. Under stress conditions, the rate of such genetic changes can increase, leading to rapid adaptation. Conversely, in hybrids formed between lineages of the chytridiomycete frog pathogen Batrachochytrium dendrobatidis (Bd), the parental genotypes are considerably less diverged (0.2% divergent). Bd hybrids are formed from crosses between lineages that rarely undergo sex. A common theme in both species is that hybrids show genome plasticity via aneuploidy or loss of heterozygosity and leverage these mechanisms as a rapid way to generate genotypic/phenotypic diversity. Some hybrids show greater fitness and survival in both virulence and virulence-associated phenotypes than parental lineages under certain conditions. These studies showcase how experimentation in model species such as Cryptococcus can be a powerful tool in elucidating the genotypic and phenotypic consequences of hybridization.


2020 ◽  
Vol 12 (4) ◽  
pp. 396-406 ◽  
Author(s):  
Uthayakumar Muthukumarasamy ◽  
Matthias Preusse ◽  
Adrian Kordes ◽  
Michal Koska ◽  
Monika Schniederjans ◽  
...  

Abstract Extensive use of next-generation sequencing has the potential to transform our knowledge on how genomic variation within bacterial species impacts phenotypic versatility. Because different environments have unique selection pressures, they drive divergent evolution. However, there is also parallel or convergent evolution of traits in independent bacterial isolates inhabiting similar environments. The application of tools to describe population-wide genomic diversity provides an opportunity to measure the predictability of genetic changes underlying adaptation. Here, we describe patterns of sequence variations in the core genome among 99 individual Pseudomonas aeruginosa clinical isolates and identified single-nucleotide polymorphisms that are the basis for branching of the phylogenetic tree. We also identified single-nucleotide polymorphisms that were acquired independently, in separate lineages, and not through inheritance from a common ancestor. Although our results demonstrate that the Pseudomonas aeruginosa core genome is highly conserved and in general, not subject to adaptive evolution, instances of parallel evolution will provide an opportunity to uncover genetic changes that underlie phenotypic diversity.


2014 ◽  
Vol 68 (1) ◽  
pp. 8-15
Author(s):  
Lena Kakasheva-Mazhenkovska ◽  
Vesna Janevska ◽  
Gordana Petrushevska ◽  
Liljana Spasevska ◽  
Neli Basheska

Abstract The stroma of the neoplasm is a highly complex structure built by: specialized mesenchymal cells typical for each tissue surroundings, cancer associated fibroblast/myofibroblast, congenital or acquired immune cells, vascular network with endothelial cells and pericytes, mastocytes, macrophages, leukocytes and adipocytes, all together incorporated in the extracellular matrix. Each neoplasm produces its own unique microenvironment where the tumor grows and modifies. Although most of the cells of the host in the stroma have compulsory tumor suppressor ability, the stroma is changing during the malignant process and it even promotes growth, invasion and metastasis. Genetic changes that occur during the development of the cancer, which are guided by the malignant cells lead to changes in the stroma of the host that will overtake it and adjust it to their own needs. In the early stages of the tumor development and invasion, the basal membrane is degraded and the stroma becomes active and contains an increased number of fibroblasts, inflammatory infiltrate and newly composed capillaries which come into direct contact with the tumor cells. These changes lead to cancer invasion.


Author(s):  
В.А. Бывальцев ◽  
И.А. Степанов ◽  
Е.Г. Белых ◽  
А.И. Яруллина

Цель обзора - анализ современных данных литературы о нарушении внутриклеточных сигнальных путей, играющих ведущую роль в развитии менингиом, генетических и молекулярных профилях данной группы опухолей. К настоящему времени изучено множество аберрантных сигнальных внутриклеточных путей, которые играют важнейшую роль в развитии менингиом головного мозга. Четкое понимание поврежденных внутриклеточных каскадов поможет изучить влияние генетических мутаций и их эффектов на менингиомогенез. Подробное исследование генетического и молекулярного профиля менингиом позволит сделать первый уверенный шаг в разработке более эффективных методов лечения данной группы интракраниальных опухолей. Хромосомы 1, 10, 14, 22 и связанные с ними генные мутации ответственны за рост и прогрессию менингиом. Предполагается, что только через понимание данных генетических повреждений будут реализованы новейшие эффективные методы лечения. Будущая терапия будет включать в себя комбинации таргетных молекулярных агентов, в том числе генную терапию, малые интерферирующие РНК, протонную терапию и другие методы воздействия, как результат дальнейшего изучения генетических и биологических изменений, характерных для менингеальных опухолей. Meningiomas are by far the most common tumors arising from the meninges. A myriad of aberrant signaling pathways involved with meningioma tumorigenesis, have been discovered. Understanding these disrupted pathways will aid in deciphering the relationship between various genetic changes and their downstream effects on meningioma pathogenesis. An understanding of the genetic and molecular profile of meningioma would provide a valuable first step towards developing more effective treatments for this intracranial tumor. Chromosomes 1, 10, 14, 22, their associated genes, have been linked to meningioma proliferation and progression. It is presumed that through an understanding of these genetic factors, more educated meningioma treatment techniques can be implemented. Future therapies will include combinations of targeted molecular agents including gene therapy, si-RNA mediation, proton therapy, and other approaches as a result of continued progress in the understanding of genetic and biological changes associated with meningiomas.


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