Current Genomics (CURR GENOMICS)

Publications in this journal

• Article: Compatible Solute Engineering in Plants for Abiotic Stress Tolerance - Role of Glycine Betaine

  Shabir Hussain Wani, Naorem Brajendra Singh, Athokpam Haribhushan, Javed Iqbal Mir
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  ABSTRACT: Abiotic stresses collectively are responsible for crop losses worldwide. Among these, drought and salinity are the most destructive. Different strategies have been proposed for management of these stresses. Being a complex trait, conventional breeding approaches have resulted in less success. Biotechnology has emerged as an additional and novel tool for deciphering the mechanism behind these stresses. The role of compatible solutes in abiotic stress tolerance has been studied extensively. Osmotic adjustment, at the physiological level, is an adaptive mechanism involved in drought or salinity tolerance, which permits the maintenance of turgor under conditions of water deficit, as it can counteract the effects of a rapid decline in leaf water potential. Increasing evidence from a series of in vivo and in vitro studies of the physiology, biochemistry, genetics, and molecular biology of plants suggest strongly that Glycine Betaine (GB) performs an important function in plants subjected to environmental stresses. It plays an adaptive role in mediating osmotic adjustment and protecting the sub-cellular structures in stressed plants, protection of the transcriptional and translational machineries and intervention as a molecular chaperone in the refolding of enzymes. Many important crops like rice do not accumulate glycinebetaine under stress conditions. Both the exogenous application of GB and the genetically engineered biosynthesis of GB in such crops is a promising strategy to increase stress tolerance. In this review we will discuss the importance of GB for abiotic stress tolerance in plants. Further, strategies like exogenic application and transgenic development of plants accumulating GB will be also be discussed. Work done on exogenic application and genetically engineered biosynthesis of GB will be listed and its advantages and limitations will be described.
  Current Genomics 05/2013; 14(3):157-165.
• Article: Role of the Transforming-Growth-Factor-1 Gene in Late-Onset Alzheimers Disease: Implications for the Treatment

  P Bosco, R Ferri, M Grazia Salluzzo, S Castellano, M Signorelli, F Nicoletti, Santo Di Nuovo, Filippo Drago, Filippo Caraci
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  ABSTRACT: Late-onset Alzheimer's disease (LOAD) is the most common form of dementia in the elderly. LOAD has a complex and largely unknown etiology with strong genetic determinants. Genetics of LOAD is known to involve several genetic risk factors among which the Apolipoprotein E (APOE) gene seems to be the major recognized genetic determinant. Recent efforts have been made to identify other genetic factors involved in the pathophysiology of LOAD such as genes associated with a deficit of neurotrophic factors in the AD brain. Genetic variations of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), and transforming-growth-factor-β1 (TGF-β1) are known to increase the risk to develop LOAD and have also been related to depression susceptibility in LOAD. Transforming-Growth-Factor-β1 (TGF- β1) is a neurotrophic factor that exerts neuroprotective effects against β-amyloid-induced neurodegeneration. Recent evidence suggests that a specific impairment in the signaling of TGF-β is an early event in the pathogenesis of AD. TGF-β1 protein levels are predominantly under genetic control, and the TGF-β1 gene, located on chromosome 19q13.1-3, contains several single nucleotide polymorphisms (SNPs) upstream and in the transcript region, such as the SNP at codon +10 (T/C) and +25 (G/C), which is known to influence the level of expression of TGF-β1. In the present review, we summarize the current literature on genetic risk factors for LOAD, focusing on the role of the TGF-β1 gene, finally discussing the possible implications of these genetic studies for the selection of patients eligible for neuroprotective strategies in AD.
  Current Genomics 04/2013; 14(2):147-156.
• Article: Integrated Analysis of Transcriptomic and Proteomic Data

  Saad Haider, Ranadip Pal
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  ABSTRACT: http://www.eurekaselect.com/107606/article
  Current Genomics 03/2013; 14(2):91-110.
• Article: Genome-Wide RNAi Longevity Screens in Caenorhabditis elegans.

  Melana E Yanos, Christopher F Bennett, Matt Kaeberlein
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  ABSTRACT: Progress in aging research has identified genetic and environmental factors that regulate longevity across species. The nematode worm Caenorhabditis elegans is a genetically tractable model system that has been widely used to investigate the molecular mechanisms of aging, and the development of RNA interference (RNAi) technology has provided a powerful tool for performing large-scale genetic screens in this organism. Genome-wide screens have identified hundreds of genes that influence lifespan, many of which fall into distinct functional classes and pathways. The purpose of this review is to summarize the results of large-scale RNAi longevity screens in C. elegans, and to provide an in-depth comparison and analysis of their methodology and most significant findings.
  Current Genomics 11/2012; 13(7):508-18.
• Article: Genome-scale studies of aging: challenges and opportunities.

  Mark A McCormick, Brian K Kennedy
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  ABSTRACT: Whole-genome studies involving a phenotype of interest are increasingly prevalent, in part due to a dramatic increase in speed at which many high throughput technologies can be performed coupled to simultaneous decreases in cost. This type of genome-scale methodology has been applied to the phenotype of lifespan, as well as to whole-transcriptome changes during the aging process or in mutants affecting aging. The value of high throughput discovery-based science in this field is clearly evident, but will it yield a true systems-level understanding of the aging process? Here we review some of this work to date, focusing on recent findings and the unanswered puzzles to which they point. In this context, we also discuss recent technological advances and some of the likely future directions that they portend.
  Current Genomics 11/2012; 13(7):500-7.
• Article: Genetic association studies: an information content perspective.

  Cen Wu, Shaoyu Li, Yuehua Cui
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  ABSTRACT: The availability of high-density single nucleotide polymorphisms (SNPs) data has made the human genetic association studies possible to identify common and rare variants underlying complex diseases in a genome-wide scale. A handful of novel genetic variants have been identified, which gives much hope and prospects for the future of genetic association studies. In this process, statistical and computational methods play key roles, among which information-based association tests have gained large popularity. This paper is intended to give a comprehensive review of the current literature in genetic association analysis casted in the framework of information theory. We focus our review on the following topics: (1) information theoretic approaches in genetic linkage and association studies; (2) entropy-based strategies for optimal SNP subset selection; and (3) the usage of theoretic information criteria in gene clustering and gene regulatory network construction.
  Current Genomics 11/2012; 13(7):566-73.
• Article: Genomics and genetics of aging.

  Matt Kaeberlein
  Current Genomics 11/2012; 13(7):499.
• Article: Systems biology in aging: linking the old and the young.

  Lei Hou, Jialiang Huang, Christopher D Green, Jerome Boyd-Kirkup, Wei Zhang, Xiaoming Yu, Wenxuan Gong, Bing Zhou, Jing-Dong J Han
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  ABSTRACT: Aging can be defined as a process of progressive decline in the physiological capacity of an organism, manifested by accumulated alteration and destabilization at the whole system level. Systems biology approaches offer a promising new perspective to examine the old problem of aging. We begin this review by introducing the concepts of systems biology, and then illustrate the application of systems biology approaches to aging research, from gene expression profiling to network analysis. We then introduce the network that can be constructed using known lifespan and aging regulators, and conclude with a look forward to the future of systems biology in aging research. In summary, systems biology is not only a young field that may help us understand aging at a higher level, but also an important platform that can link different levels of knowledge on aging, moving us closer to a more comprehensive control of systematic decline during aging.
  Current Genomics 11/2012; 13(7):558-65.
• Article: On the limitations of biological knowledge.

  Edward R Dougherty, Ilya Shmulevich
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  ABSTRACT: Scientific knowledge is grounded in a particular epistemology and, owing to the requirements of that epistemology, possesses limitations. Some limitations are intrinsic, in the sense that they depend inherently on the nature of scientific knowledge; others are contingent, depending on the present state of knowledge, including technology. Understanding limitations facilitates scientific research because one can then recognize when one is confronted by a limitation, as opposed to simply being unable to solve a problem within the existing bounds of possibility. In the hope that the role of limiting factors can be brought more clearly into focus and discussed, we consider several sources of limitation as they apply to biological knowledge: mathematical complexity, experimental constraints, validation, knowledge discovery, and human intellectual capacity.
  Current Genomics 11/2012; 13(7):574-87.
• Article: Chromatin remodeling, DNA damage repair and aging.

  Baohua Liu, Raymond Kh Yip, Zhongjun Zhou
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  ABSTRACT: Cells are constantly exposed to a variety of environmental and endogenous conditions causing DNA damage, which is detected and repaired by conserved DNA repair pathways to maintain genomic integrity. Chromatin remodeling is critical in this process, as the organization of eukaryotic DNA into compact chromatin presents a natural barrier to all DNA-related events. Studies on human premature aging syndromes together with normal aging have suggested that accumulated damages might lead to exhaustion of resources that are required for physiological functions and thus accelerate aging. In this manuscript, combining the present understandings and latest findings, we focus mainly on discussing the role of chromatin remodeling in the repair of DNA double-strand breaks (DSBs) and regulation of aging.
  Current Genomics 11/2012; 13(7):533-47.
• Article: MicroRNA in Aging: From Discovery to Biology.

  Hwa Jin Jung, Yousin Suh
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  ABSTRACT: MicroRNAs (miRNAs) are small non-coding RNA molecules that negatively regulate gene expression of their targets at the post-transcriptional levels. A single miRNA can target up to several hundred mRNAs, thus capable of significantly altering gene expression regulatory networks. In-depth study and characterization of miRNAs has elucidated their critical functions in development, homeostasis, and disease. A link between miRNAs and longevity has been demonstrated in C. elegans, implicating their role in regulation of lifespan and in the aging process. Recent years have witnessed unprecedented technological advances in studies of miRNAs, including ultra-high throughput sequencing technologies that allow comprehensive discovery of miRNAs and their targets. Here we review the latest experimental approaches from the perspective of understanding miRNA gene expression regulatory networks in aging. We provide a methodological work flow that can be employed to discover aging-related miRNAs and their targets, and to functionally validate their roles in aging. Finally, we review the links between miRNAs known to act in the conserved pathways of aging and major aging-related diseases. Taken together, we hope to provide a focused review to facilitate future endeavor of uncovering the functional role of miRNA in aging.
  Current Genomics 11/2012; 13(7):548-57.
• Article: Mitochondria and organismal longevity.

  Ara B Hwang, Dae-Eun Jeong, Seung-Jae Lee
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  ABSTRACT: Mitochondria are essential for various biological processes including cellular energy production. The oxidative stress theory of aging proposes that mitochondria play key roles in aging by generating reactive oxygen species (ROS), which indiscriminately damage macromolecules and lead to an age-dependent decline in biological function. However, recent studies show that increased levels of ROS or inhibition of mitochondrial function can actually delay aging and increase lifespan. The aim of this review is to summarize recent findings regarding the role of mitochondria in organismal aging processes. We will discuss how mitochondria contribute to evolutionarily conserved longevity pathways, including mild inhibition of respiration, dietary restriction, and target of rapamycin (TOR) signaling.
  Current Genomics 11/2012; 13(7):519-32.
• Article: Single cell genomics of the brain: focus on neuronal diversity and neuropsychiatric diseases. Iourov IY, Vorsanova SG, Yurov YB. Curr Genomics. 2012 Sep;13(6):477-88. doi: 10.2174/138920212802510439.

  Iourov IY, Vorsanova SG, Yurov YB
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  ABSTRACT: Single cell genomics of the brain: focus on neuronal diversity and neuropsychiatric diseases. Iourov IY, Vorsanova SG, Yurov YB. Curr Genomics. 2012 Sep;13(6):477-88. doi: 10.2174/138920212802510439.
  Current Genomics 09/2012;
• Article: On the Power of Additional and Complex Chromosomal Aberrations in CML.

  Karin M Greulich-Bode, Barbara Heinze
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  ABSTRACT: Unregulated proliferation of mainly myeloid bone marrow cells and genetic changes in the hematopoietic stem cell system are important features in Chronic Myeloid Leukemia (CML). In clinical diagnosis of CML, classical banding techniques, fluorescence in situ hybridization (FISH) probing for the Philadelphia chromosome (Ph) or polymerase chain reaction amplifying the fusion products of the BCR-ABL fusion are state of the art techniques. Nevertheless, the genome of CML patients harbors many more cytogenetic changes. These might be hidden in subpopulations due to clonal events or involved in extremely complex aberrations. To identify these additional changes, several cytogenetic and molecular genetic techniques could be applied. Nevertheless, it has been proposed that identifying these aberrations is time consuming and costly and since they cannot be converted into a benefit for the patients, the necessity to perform these investigations has been questioned. In the times where highly specialized medicine is advancing into several areas of cancer, this attitude needs to be reassessed. Therefore, we looked at the usefulness of a combination of different techniques to unravel the genetic changes in CML patients and to identify new chromosomal aberrations, which potentially can be correlated to different stages of the disease and the strength of therapy resistance. We are convinced that the combination of these techniques could be extremely useful in unraveling even the most complex karyotypes and in dissecting different clones contributing to the disease. We propose that by doing so, this would improve CML diagnostic and prognostic findings, especially with regard to CML resistance mechanisms and new therapeutic strategies.
  Current Genomics 09/2012; 13(6):471-6.
• Article: Single cell genomics of the brain: focus on neuronal diversity and neuropsychiatric diseases.

  Ivan Y Iourov, Svetlana G Vorsanova, Yuri B Yurov
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  ABSTRACT: Single cell genomics has made increasingly significant contributions to our understanding of the role that somatic genome variations play in human neuronal diversity and brain diseases. Studying intercellular genome and epigenome variations has provided new clues to the delineation of molecular mechanisms that regulate development, function and plasticity of the human central nervous system (CNS). It has been shown that changes of genomic content and epigenetic profiling at single cell level are involved in the pathogenesis of neuropsychiatric diseases (schizophrenia, mental retardation (intellectual/leaning disability), autism, Alzheimer's disease etc.). Additionally, several brain diseases were found to be associated with genome and chromosome instability (copy number variations, aneuploidy) variably affecting cell populations of the human CNS. The present review focuses on the latest advances of single cell genomics, which have led to a better understanding of molecular mechanisms of neuronal diversity and neuropsychiatric diseases, in the light of dynamically developing fields of systems biology and "omics".
  Current Genomics 09/2012; 13(6):477-88.
• Article: Characterization of the early CNS stress biomarkers and profiles associated with neuropsychiatric diseases.

  Xr Lowe, Aj Wyrobek
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  ABSTRACT: Neuropsychiatric disorders (including dementia) have high personal, family, and social costs. Although many neuropsychiatric disorders share common patterns of symptoms and treatments, there are no validated biomarkers that define the underlying molecular mechanisms in the central nervous system (CNS). We hypothesize that there are early and common molecular changes in the CNS that will serve as sensitive indicators of CNS molecular stress and that will be predictive of neuropathological changes resulted in increasing the risk for neuropsychiatric diseases. Using the rodent model, we showed that systemic exposure to three diverse CNS stressors with different mechanisms of action (ketamine, low-dose and high-dose ionizing radiation, interferon-α) induced the expression of troponin T1 (Tnnt 1) within hours in adult mouse brain tissue. Tnnt 1 expression was induced in neuronal (not glial) cells, the hippocampal zone of neurogenesis, cerebral cortex, amygdale, and choroid plexus, which are important CNS locations in behavior and mental health. We also identified nine neural signaling pathways that showed a high degree of concordance in their transcriptional response in mouse brain tissue for hours after low-dose irradiation, in the aging human brain (unirradiated), and in brain tissue from patients with Alzheimer's disease. Our studies provide new molecular information on shared mechanisms and expression profiles of diverse neuropsychiatric disorders. This knowledge will be fundamental for developing molecular signatures of early CNS stress biomarker for early diagnosis and treatment of neuropsychiatric diseases.
  Current Genomics 09/2012; 13(6):489-97.
• Article: Current genomics in cardiovascular medicine.

  Vinit Sawhney, Scott Brouilette, Dominic Abrams, Richard Schilling, Benjamin O'Brien
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  ABSTRACT: Cardiovascular disease (CVD) is a heterogeneous, complex trait that has a major impact on human morbidity and mortality. Common genetic variation may predispose to common forms of CVD in the community, and rare genetic conditions provide unique pathogenetic insights into these diseases. With the advent of the Human Genome Project and the genomic era, new tools and methodologies have revolutionised the field of genetic research in cardiovascular medicine. In this review, we describe the rationale for the current emphasis on large-scale genomic studies, elaborate on genome wide association studies and summarise the impact of genomics on clinical cardiovascular medicine and how this may eventually lead to new therapeutics and personalised medicine.
  Current Genomics 09/2012; 13(6):446-62.