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Biology, Volume 3, Issue 3 (September 2014), Pages 452-644

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Research

Jump to: Review, Other

Open AccessArticle Development of a Functionally Minimized Mutant of the R3C Ligase Ribozyme Offers Insight into the Plausibility of the RNA World Hypothesis
Biology 2014, 3(3), 452-465; doi:10.3390/biology3030452
Received: 9 June 2014 / Revised: 14 July 2014 / Accepted: 22 July 2014 / Published: 29 July 2014
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Abstract
The R3C ligase ribozyme is an artificial ligase ribozyme produced by modification of the ribozyme that lacks cytidine. Here, we attempted to modify the original R3C ribozyme (73 nucleotides) by reducing the number of nucleotides while maintaining the maximum possible catalytic efficiency. By
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The R3C ligase ribozyme is an artificial ligase ribozyme produced by modification of the ribozyme that lacks cytidine. Here, we attempted to modify the original R3C ribozyme (73 nucleotides) by reducing the number of nucleotides while maintaining the maximum possible catalytic efficiency. By partially deleting both the “grip” (P4 + P5) and “hammer” (P3) stem-loops, we found the critical border to retain activity comparable to that of full-length R3C. The three-way junction structure was necessary to maintain enzymatic function and the stability of the “grip” (P4 + P5) stem had a large influence on the catalytic activity of R3C. The final minimized ribozyme we obtained comprised ~50 nucleotides, comparable to the estimated length of prebiotically synthesized RNA. Our findings suggest that the autocatalytic function in ribozymes is indeed possible to obtain using sequence lengths achievable with prebiotic synthesis. Full article
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Open AccessArticle The Distribution and Identity of Edaphic Fungi in the McMurdo Dry Valleys
Biology 2014, 3(3), 466-483; doi:10.3390/biology3030466
Received: 23 May 2014 / Revised: 14 July 2014 / Accepted: 16 July 2014 / Published: 30 July 2014
Cited by 7 | PDF Full-text (1095 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Contrary to earlier assumptions, molecular evidence has demonstrated the presence of diverse and localized soil bacterial communities in the McMurdo Dry Valleys of Antarctica. Meanwhile, it remains unclear whether fungal signals so far detected in Dry Valley soils using both culture-based and molecular
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Contrary to earlier assumptions, molecular evidence has demonstrated the presence of diverse and localized soil bacterial communities in the McMurdo Dry Valleys of Antarctica. Meanwhile, it remains unclear whether fungal signals so far detected in Dry Valley soils using both culture-based and molecular techniques represent adapted and ecologically active biomass or spores transported by wind. Through a systematic and quantitative molecular survey, we identified significant heterogeneities in soil fungal communities across the Dry Valleys that robustly correlate with heterogeneities in soil physicochemical properties. Community fingerprinting analysis and 454 pyrosequencing of the fungal ribosomal intergenic spacer region revealed different levels of heterogeneity in fungal diversity within individual Dry Valleys and a surprising abundance of Chytridiomycota species, whereas previous studies suggested that Dry Valley soils were dominated by Ascomycota and Basidiomycota. Critically, we identified significant differences in fungal community composition and structure of adjacent sites with no obvious barrier to aeolian transport between them. These findings suggest that edaphic fungi of the Antarctic Dry Valleys are adapted to local environments and represent an ecologically relevant (and possibly important) heterotrophic component of the ecosystem. Full article
Open AccessArticle Vesicular Trafficking Defects, Developmental Abnormalities, and Alterations in the Cellular Death Process Occur in Cell Lines that Over-Express Dictyostelium GTPase, Rab2, and Rab2 Mutants
Biology 2014, 3(3), 514-535; doi:10.3390/biology3030514
Received: 18 June 2014 / Revised: 29 July 2014 / Accepted: 13 August 2014 / Published: 25 August 2014
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Abstract
Small molecular weight GTPase Rab2 has been shown to be a resident of pre-Golgi intermediates and required for protein transport from the ER to the Golgi complex, however, the function of Rab2 in Dictyostelium has yet to be fully characterized. Using cell
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Small molecular weight GTPase Rab2 has been shown to be a resident of pre-Golgi intermediates and required for protein transport from the ER to the Golgi complex, however, the function of Rab2 in Dictyostelium has yet to be fully characterized. Using cell lines that over-express DdRab2, as well as cell lines over-expressing constitutively active (CA), and dominant negative (DN) forms of the GTPase, we report a functional role in vesicular transport specifically phagocytosis, and endocytosis. Furthermore, Rab2 like other GTPases cycles between an active GTP-bound and an inactive GDP-bound state. We found that this GTP/GDP cycle for DdRab2 is crucial for normal Dictyostelium development and cell–cell adhesion. Similar to Rab5 and Rab7 in C. elegans, we found that DdRab2 plays a role in programmed cell death, possibly in the phagocytic removal of apoptotic corpses. Full article
Open AccessArticle Genetic Risk Scores Associated with Baseline Lipoprotein Subfraction Concentrations Do Not Associate with Their Responses to Fenofibrate
Biology 2014, 3(3), 536-550; doi:10.3390/biology3030536
Received: 23 June 2014 / Revised: 29 July 2014 / Accepted: 5 August 2014 / Published: 25 August 2014
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Abstract
Lipoprotein subclass concentrations are modifiable markers of cardiovascular disease risk. Fenofibrate is known to show beneficial effects on lipoprotein subclasses, but little is known about the role of genetics in mediating the responses of lipoprotein subclasses to fenofibrate. A recent genomewide association study
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Lipoprotein subclass concentrations are modifiable markers of cardiovascular disease risk. Fenofibrate is known to show beneficial effects on lipoprotein subclasses, but little is known about the role of genetics in mediating the responses of lipoprotein subclasses to fenofibrate. A recent genomewide association study (GWAS) associated several single nucleotide polymorphisms (SNPs) with lipoprotein measures, and validated these associations in two independent populations. We used this information to construct genetic risk scores (GRSs) for fasting lipoprotein measures at baseline (pre-fenofibrate), and aimed to examine whether these GRSs also associated with the responses of lipoproteins to fenofibrate. Fourteen lipoprotein subclass measures were assayed in 817 men and women before and after a three week fenofibrate trial. We set significance at a Bonferroni corrected alpha <0.05 (p < 0.004). Twelve subclass measures changed with fenofibrate administration (each p = 0.003 to <0.0001). Mixed linear models which controlled for age, sex, body mass index (BMI), smoking status, pedigree and study-center, revealed that GRSs were associated with eight baseline lipoprotein measures (p < 0.004), however no GRS was associated with fenofibrate response. These results suggest that the mechanisms for changes in lipoprotein subclass concentrations with fenofibrate treatment are not mediated by the genetic risk for fasting levels. Full article
(This article belongs to the Special Issue Lipid Metabolism)

Review

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Open AccessReview Control of Glycosylation-Related Genes by DNA Methylation: the Intriguing Case of the B3GALT5 Gene and Its Distinct Promoters
Biology 2014, 3(3), 484-497; doi:10.3390/biology3030484
Received: 28 April 2014 / Revised: 22 July 2014 / Accepted: 25 July 2014 / Published: 4 August 2014
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Abstract
Glycosylation is a metabolic pathway consisting of the enzymatic modification of proteins and lipids through the stepwise addition of sugars that gives rise to glycoconjugates. To determine the full complement of glycoconjugates that cells produce (the glycome), a variety of genes are involved,
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Glycosylation is a metabolic pathway consisting of the enzymatic modification of proteins and lipids through the stepwise addition of sugars that gives rise to glycoconjugates. To determine the full complement of glycoconjugates that cells produce (the glycome), a variety of genes are involved, many of which are regulated by DNA methylation. The aim of the present review is to briefly describe some relevant examples of glycosylation-related genes whose DNA methylation has been implicated in their regulation and to focus on the intriguing case of a glycosyltransferase gene (B3GALT5). Aberrant promoter methylation is frequently at the basis of their modulation in cancer, but in the case of B3GALT5, at least two promoters are involved in regulation, and a complex interplay is reported to occur between transcription factors, chromatin remodelling and DNA methylation of typical CpG islands or even of other CpG dinucleotides. Transcription of the B3GALT5 gene underwent a particular evolutionary fate, so that promoter hypermethylation, acting on one transcript, and hypomethylation of other sequences, acting on the other, cooperate on one gene to obtain full cancer-associated silencing. The findings may also help in unravelling the complex origin of serum CA19.9 antigen circulating in some patients. Full article
(This article belongs to the Special Issue DNA Methylation)
Open AccessReview Preterm Birth and Its Long-Term Effects: Methylation to Mechanisms
Biology 2014, 3(3), 498-513; doi:10.3390/biology3030498
Received: 26 May 2014 / Revised: 8 August 2014 / Accepted: 12 August 2014 / Published: 21 August 2014
Cited by 7 | PDF Full-text (149 KB) | HTML Full-text | XML Full-text
Abstract
The epigenetic patterns established during development may influence gene expression over a lifetime and increase susceptibility to chronic disease. Being born preterm (<37 weeks of gestation) is associated with increased risk mortality and morbidity from birth until adulthood. This brief review explores the
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The epigenetic patterns established during development may influence gene expression over a lifetime and increase susceptibility to chronic disease. Being born preterm (<37 weeks of gestation) is associated with increased risk mortality and morbidity from birth until adulthood. This brief review explores the potential role of DNA methylation in preterm birth (PTB) and its possible long-term consequences and provides an overview of the physiological processes central to PTB and recent DNA methylation studies of PTB. Full article
(This article belongs to the Special Issue DNA Methylation)
Open AccessReview Regulated DNA Methylation and the Circadian Clock: Implications in Cancer
Biology 2014, 3(3), 560-577; doi:10.3390/biology3030560
Received: 7 May 2014 / Revised: 12 August 2014 / Accepted: 15 August 2014 / Published: 5 September 2014
Cited by 6 | PDF Full-text (1037 KB) | HTML Full-text | XML Full-text
Abstract
Since the cloning and discovery of DNA methyltransferases (DNMT), there has been a growing interest in DNA methylation, its role as an epigenetic modification, how it is established and removed, along with the implications in development and disease. In recent years, it has
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Since the cloning and discovery of DNA methyltransferases (DNMT), there has been a growing interest in DNA methylation, its role as an epigenetic modification, how it is established and removed, along with the implications in development and disease. In recent years, it has become evident that dynamic DNA methylation accompanies the circadian clock and is found at clock genes in Neurospora, mice and cancer cells. The relationship among the circadian clock, cancer and DNA methylation at clock genes suggests a correlative indication that improper DNA methylation may influence clock gene expression, contributing to the etiology of cancer. The molecular mechanism underlying DNA methylation at clock loci is best studied in the filamentous fungi, Neurospora crassa, and recent data indicate a mechanism analogous to the RNA-dependent DNA methylation (RdDM) or RNAi-mediated facultative heterochromatin. Although it is still unclear, DNA methylation at clock genes may function as a terminal modification that serves to prevent the regulated removal of histone modifications. In this capacity, aberrant DNA methylation may serve as a readout of misregulated clock genes and not as the causative agent. This review explores the implications of DNA methylation at clock loci and describes what is currently known regarding the molecular mechanism underlying DNA methylation at circadian clock genes. Full article
(This article belongs to the Special Issue DNA Methylation)
Open AccessReview Dnmt3b Prefers Germ Line Genes and Centromeric Regions: Lessons from the ICF Syndrome and Cancer and Implications for Diseases
Biology 2014, 3(3), 578-605; doi:10.3390/biology3030578
Received: 18 May 2014 / Revised: 18 July 2014 / Accepted: 21 August 2014 / Published: 5 September 2014
Cited by 6 | PDF Full-text (1000 KB) | HTML Full-text | XML Full-text
Abstract
The correct establishment and maintenance of DNA methylation patterns are critical for mammalian development and the control of normal cell growth and differentiation. DNA methylation has profound effects on the mammalian genome, including transcriptional repression, modulation of chromatin structure, X chromosome inactivation, genomic
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The correct establishment and maintenance of DNA methylation patterns are critical for mammalian development and the control of normal cell growth and differentiation. DNA methylation has profound effects on the mammalian genome, including transcriptional repression, modulation of chromatin structure, X chromosome inactivation, genomic imprinting, and the suppression of the detrimental effects of repetitive and parasitic DNA sequences on genome integrity. Consistent with its essential role in normal cells and predominance at repetitive genomic regions, aberrant changes of DNA methylation patterns are a common feature of diseases with chromosomal and genomic instabilities. In this context, the functions of DNA methyltransferases (DNMTs) can be affected by mutations or alterations of their expression. DNMT3B, which is involved in de novo methylation, is of particular interest not only because of its important role in development, but also because of its dysfunction in human diseases. Expression of catalytically inactive isoforms has been associated with cancer risk and germ line hypomorphic mutations with the ICF syndrome (Immunodeficiency Centromeric instability Facial anomalies). In these diseases, global genomic hypomethylation affects repeated sequences around centromeric regions, which make up large blocks of heterochromatin, and is associated with chromosome instability, impaired chromosome segregation and perturbed nuclear architecture. The review will focus on recent data about the function of DNMT3B, and the consequences of its deregulated activity on pathological DNA hypomethylation, including the illicit activation of germ line-specific genes and accumulation of transcripts originating from repeated satellite sequences, which may represent novel physiopathological biomarkers for human diseases. Notably, we focus on cancer and the ICF syndrome, pathological contexts in which hypomethylation has been extensively characterized. We also discuss the potential contribution of these deregulated protein-coding and non-coding transcription programs to the perturbation of cellular phenotypes. Full article
(This article belongs to the Special Issue DNA Methylation)
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Open AccessReview Discerning Primary and Secondary Factors Responsible for Clinical Fatigue in Multisystem Diseases
Biology 2014, 3(3), 606-622; doi:10.3390/biology3030606
Received: 27 June 2014 / Revised: 21 August 2014 / Accepted: 1 September 2014 / Published: 22 September 2014
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Abstract
Fatigue is a common symptom of numerous acute and chronic diseases, including myalgic encephalomyelitis/chronic fatigue syndrome, multiple sclerosis, heart failure, cancer, and many others. In these multi-system diseases the physiological determinants of enhanced fatigue encompass a combination of metabolic, neurological, and myofibrillar adaptations.
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Fatigue is a common symptom of numerous acute and chronic diseases, including myalgic encephalomyelitis/chronic fatigue syndrome, multiple sclerosis, heart failure, cancer, and many others. In these multi-system diseases the physiological determinants of enhanced fatigue encompass a combination of metabolic, neurological, and myofibrillar adaptations. Previous research studies have focused on adaptations specific to skeletal muscle and their role in fatigue. However, most have neglected the contribution of physical inactivity in assessing disease syndromes, which, through deconditioning, likely contributes to symptomatic fatigue. In this commentary, we briefly review disease-related muscle phenotypes in the context of whether they relate to the primary disease or whether they develop secondary to reduced physical activity. Knowledge of the etiology of the skeletal muscle adaptations in these conditions and their contribution to fatigue symptoms is important for understanding the utility of exercise rehabilitation as an intervention to alleviate the physiological precipitants of fatigue. Full article
(This article belongs to the Special Issue Muscle Structure and Function)
Open AccessReview The Structural and Functional Coordination of Glycolytic Enzymes in Muscle: Evidence of a Metabolon?
Biology 2014, 3(3), 623-644; doi:10.3390/biology3030623
Received: 14 July 2014 / Revised: 5 September 2014 / Accepted: 8 September 2014 / Published: 22 September 2014
Cited by 3 | PDF Full-text (601 KB) | HTML Full-text | XML Full-text
Abstract
Metabolism sustains life through enzyme-catalyzed chemical reactions within the cells of all organisms. The coupling of catalytic function to the structural organization of enzymes contributes to the kinetic optimization important to tissue-specific and whole-body function. This coupling is of paramount importance in the
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Metabolism sustains life through enzyme-catalyzed chemical reactions within the cells of all organisms. The coupling of catalytic function to the structural organization of enzymes contributes to the kinetic optimization important to tissue-specific and whole-body function. This coupling is of paramount importance in the role that muscle plays in the success of Animalia. The structure and function of glycolytic enzyme complexes in anaerobic metabolism have long been regarded as a major regulatory element necessary for muscle activity and whole-body homeostasis. While the details of this complex remain to be elucidated through in vivo studies, this review will touch on recent studies that suggest the existence of such a complex and its structure. A potential model for glycolytic complexes and related subcomplexes is introduced. Full article
(This article belongs to the Special Issue Muscle Structure and Function)

Other

Jump to: Research, Review

Open AccessProject Report Elevated Circulating TNF-α in Fat-Free Mass Non-Responders Compared to Responders Following Exercise Training in Older Women
Biology 2014, 3(3), 551-559; doi:10.3390/biology3030551
Received: 24 June 2014 / Revised: 14 August 2014 / Accepted: 26 August 2014 / Published: 5 September 2014
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Abstract
The purpose of this investigation was to determine if differences in inflammatory cytokines exist between fat-free mass responders versus non-responders following a combined resistance/aerobic training program in older women. Fifty women over 60 years old, mean BMI 27 ± 4 (kg/m2)
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The purpose of this investigation was to determine if differences in inflammatory cytokines exist between fat-free mass responders versus non-responders following a combined resistance/aerobic training program in older women. Fifty women over 60 years old, mean BMI 27 ± 4 (kg/m2) and physically untrained, participated in a combined training program for 16-weeks. Body composition, muscle strength, and serum inflammatory markers (TNF-α, CRP, and IL-6) were assessed at baseline and 16-weeks post-training. A significant time effect was observed for weight, %fat, fat mass, and all strength measures (p < 0.05). A group interaction was observed for TNF-α (p < 0.05), which revealed higher concentrations of circulating TNF-α at baseline (18%) and post-exercise training (24%) in non-responders compared to responders (p < 0.05). In conclusion, this study revealed a significantly greater concentration of circulating TNF-α in older women that do not increase fat-free mass following training. Full article
(This article belongs to the Special Issue Muscle Structure and Function)

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