bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mechanism of Single‐Stranded
DNA
Transposition: A Structural Perspective
Authors: Barabas Orsolya 
Published: April 2013

Abstract

Transposons are mobile genetic elements that have shaped evolution and thus constitute much of modern genomes. Their movements cause diseases, change regulatory patterns and spread antibiotic resistance.
Single‐stranded deoxyribonucleic acid (ssDNA)
transposition, is carried out by a unique transposase protein that recognises a hairpin structure formed on ssDNA, excises the transposon as a single‐stranded circle, and integrates it specifically into ssDNA target. The use of ssDNA alleviates the cumbersome processing of the second DNA strand and implies a built‐in regulation of transposition via substrate limitation

in vivo

. Moreover, it allows selection of a specific sequence for integration via base‐pairing between transposon and target DNA. Due to this target site recognition strategy the transposon can be redirected to novel sites and may permit the development of programmable site‐specific genetic tools for research and gene therapy. Furthermore, unexpected similarities suggest that ssDNA transposons share mechanistic features with repetitive extragenic palindromes and
ribonucleic acid (RNA)
machines.

Key Concepts:

Transposons are mobile genetic parasites that can move from one location in the genome to another.

Transposons are abundant in most prokaryotic and eukaryotic organisms, where they contribute to genome structure, function and evolution.

Single‐stranded DNA (ssDNA) transposition is carried out solely on ssDNA substrates and intermediates.

ssDNA transposons alleviate the need for cutting and pasting two DNA strands and thereby preserve chemical energy.

The transposon encodes a transposase protein, which recognises, cleaves and integrates the two ends of the transposon in the context of a synaptic complex called the transpososome.

The ssDNA transpososome recognises its target site sequence specifically via base‐pairing interactions between a part of the transposon DNA and the cleavage site.

In vivo
, ssDNA transposition is limited by the availability of ssDNA, which provides a built‐in regulatory mechanism.

Their mechanism of target site recognition allows ssDNA transposons to be redirected to novel target site sequences, potentially allowing the development of unique genetic tools for research and medicine.

Repetitive extragenic palindromes (REPs) may have derived from ssDNA transposons.

In complex with a helper protein, ssDNA can form complex intertwined tertiary structures providing unique functions that were previously seen only for RNA.
Capsid‐Less
RNA
Viruses
Authors: Dolja Valerian V , Koonin Eugene V 
Published: April 2013

Abstract

Capsid‐less RNA viruses comprise an assemblage of diverse virus‐like agents with genomes of variable size that share only the gene encoding the RNA‐dependent RNA polymerase. Although double‐stranded
ribonucleic acid
(RNA) is the dominant form of virus‐specific RNA isolated from organisms infected by most capsid‐less viruses, these viruses probably have evolved independently from distinct positive‐strand RNA virus ancestors that have lost the ability to form capsids. The loss of capsid caused the loss of virus transmissibility via extracellular routes, limiting these agents to vertical transmission. The capsid‐less RNA viruses include the families
Narnaviridae, Hypoviridae
, and
Endornaviridae
as well as several viruses scattered among diverse viral lineages. The majority of the known capsid‐less viruses reproduce in fungi, and the rest in oomycetes and plants. The narnaviruses of the genus
Mitovirus
replicate within fungal mitochondria and show evolutionary affinity to RNA bacteriophages, suggesting their potential ancient origin from viruses of bacteria that gave rise to mitochondrial endosymbiont of the ancestral eukaryote. In contrast, it seems likely that the fungal hypoviruses and plant/fungal endornaviruses have emerged more recently, via reductive evolution of eukaryotic ancestral viruses of the Picornavirus‐like and Alphavirus‐like superfamilies, respectively.

Key Concepts:

Several groups of RNA viruses infecting fungi, plants and protists lack a capsid and replicate in the form of naked RNA.

Phylogenomic analysis shows that capsid‐less viruses have evolved on many independent occasions from different groups of typical positive‐strand RNA viruses.

The driving force behind the evolution of capsid‐less viruses appears the life style of their hosts such as fungi that hampers infectivity, even for viruses possessing a capsid, and restricts viruses to vertical transmission.

Numerous members of a widespread family of capsid‐less viruses, the
Narnaviridae
, replicate within the host mitochondria and are evolutionarily related to RNA bacteriophage, revealing a direct link between viruses of bacteria and eukaryotes.
Urban Biodiversity: Patterns, Processes and Implications for Conservation
Authors: Faeth Stanley H , Saari Susanna , Bang Christofer 
Published: April 2013

AbstractAs the world becomes increasingly urbanised, more and more species either reside in cities, suburbs and exurbs or are influenced by their growth. On the bases of our literature survey, species richness and diversity of animals, especially vertebrate animals, and plants usually declines in cities. However, contrary to the prevailing notion that bird abundances usually increase in cities, studies reporting increases or decreases of bird abundances are about equal. The mechanisms underlying patterns of urban biodiversity are complex and not well‐understood. Explanations for the observed changes in species diversity and composition in cities focus on local processes involving species responses to local abiotic environmental factors and interactions with other species and regional processes, such as dispersal. Recently, metacommunity theory has been applied to urban habitats to explore the relative importance of local and regional processes. This theory also provides insights into how biodiversity can be maintained and promoted in urban areas.Key Concepts:Urbanisation creates highly fragmented, heterogeneous and altered environments that act as selective filters for urban organisms and species.Urbanisation is often associated with declines in animal and plant richness, abundance and diversity.Studies showing increases or decreases in urban bird abundances are about equal, contrary to conventional wisdom of increased bird abundances in cities.Various ecological concepts have been applied to explain urban biodiversity, including disturbance and productivity gradient hypotheses and island biogeography theory.Metacommunity theory has been used recently to ascertain relative contributions of local and regional processes to urban biodiversity.Understanding local and regional processes leads to better insights in conserving and promoting urban biodiversity.Conservation efforts depend on connections to nature; therefore, it is important to engage city‐dwellers with their urban biotas.
Telomere Dysfunction in Human Genetic Disease
Authors: Morgan Garrett , Ly Hinh 
Published: April 2013

Abstract

Telomeres are specialised
deoxyribonucleic acid
(DNA) structures that cap the ends of chromosomes to protect genomic DNA. Telomerase is the enzyme that regulates telomere length to maintain the protective functions of telomeres. A major risk factor for some human diseases is telomere and telomerase dysfunction. Bone marrow deficiency syndromes as well as diabetes, hypertension and atherosclerosis have all been linked to alterations to telomeres or mutations in telomerase genes. The precise biological mechanisms involved in most of the diseases, however, are poorly understood. Research aimed at describing the biological processes that underlie these pathologies may elucidate the precise roles that telomeres and telomerase play in the progression of these diseases. Markers of telomere dynamics, such as telomere length and screening for telomerase mutations, may have some prognostic value related to these disorders.

Key Concepts:

Telomeres are repeats of the nucleic acid sequence TTAGGG.

T‐loop structure is composed of telomeric DNA and shelterin proteins.

Telomeres help maintain genomic stability in the cell.

Progressive telomeric repeat loss occurs due to the end‐replication problem and genotoxic stress.

Telomerase in an enzyme that adds TTAGGG repeats to 3′ ends of telomeres.

Bone‐marrow failure syndromes, such as dyskeratosis congenita, aplastic anaemia and idiopathic pulmonary fibrosis have been linked to telomere and telomerase dysfunctions.

Chronic diseases such as cardiovascular disease and diabetes have also been linked to telomere alterations.

In vitro
and
in vivo
research may demonstrate the precise role telomeres play in these disease processes.

In vivo
studies may lead to development of diagnostic markers and therapies for these diseases.
Protein Disorder and Human Genetic Disease
Authors: Uversky Vladimir N , Iakoucheva Lilia M , Dunker A Keith 
Published: April 2013

AbstractIntrinsically disordered proteins (IDPs) are biologically active proteins that lack stable structure under physiological conditions. They are involved in crucial biological functions related to regulation, recognition, signalling and control of various events in the cell. Misbehaviour of IDPs is commonly associated with various human diseases. IDPs represent a prominent part of the human diseasome, a network that links the human disease phenome (which includes all the human genetic diseases) with the human disease genome (which contains all the disease‐related genes), where they could be grouped into a unique entity, the human‐genetic‐disease‐associated unfoldome. The exonic single nucleotide variations (SNVs) may induce a significant change in the tendency of a protein region to be structured or disordered, thereby causing malfunction of such a protein and contributing to the disease risk. Therefore, IDPs are abundant in genetic diseases, play crucial roles in pathogenesis of these maladies, and clearly require special attention.Key Concepts:Intrinsically disordered proteins (IDPs) are common in various proteomes, where they constitute functionally broad and densely populated unfoldomes.IDPs have crucial biological functions and are responsible for regulation, recognition, signalling and control of various events in the cell.Dysfunction, dysregulation and misbehaviour of IDPs are related to the pathogenesis of various diseases.Mutations in IDPs are frequently associated with genetic diseases.Mutations affecting the potential post‐translational modification sites (which are frequently located within the intrinsically disordered regions) are often related to various diseases.A more‐detailed understanding of the roles of intrinsically disordered proteins in genetic diseases might provide a basis for rational drug design against them.
Ecology and Social Organisation of Wasps
Authors: Bell Emily , Sumner Seirian 
Published: April 2013

AbstractUnderstanding sociality is a general question in biology: it tells us how groups evolve and function, from cells to insect societies. The social wasps (Hymenoptera and Vespidae) display a wide range of diversity in their ecology and social organisation, providing insights into the origins of simple societies and the elaboration and maintenance of complex societies. Social wasps play an important role in our ecosystems and economies, for example, through their pollination and pest control services. Compared with other social insects (e.g. ants, termites and bees), the social wasps are understudied. Here the authors give a brief overview of the social wasps, their phylogenetic history, diversity in social organisation and explain how they offer important insights on the key innovations underpinning the evolution of sociality.Key Concepts:Wasps make up a huge group of social insects, yet only one‐fifth of them exhibit social behaviour.Social wasps are ideal and unique models for studying social evolution as they show the full spectrum of social organisation and behaviours.Across the social spectrum, wasp species show a number of key innovations that have contributed to their success, including the transition to group living, the evolution of castes, policing and swarm founding.The evolution of caste differentiation has led to mutual dependency between phenotypes within species, and this is likely to have facilitated increased social complexity.Studying both proximate and ultimate factors of social evolution will allow us to better understand the mechanisms of social evolution in wasps and reduce confusion in the theory of sociobiology.
Marine Protected Areas
Authors: Claudet Joachim 
Published: April 2013

Abstract

Human‐induced disturbance can affect the ecological functioning of coastal areas and reduce the associated goods and services required for human welfare. Major concerns are rising over observed declines in the abundance of particular species as well as reductions in functional diversity and changes in food web structure. As a result, the conservation and restoration of marine biodiversity and functions is a major concern. Marine protected areas are a useful management tool to mitigate some of the human‐induced changes in marine ecosystems. If properly managed and enforced, they can have several ecological, fisheries and socio‐economic benefits. Effects of marine protected areas are variable and context‐dependent but main drivers of change are now known. In recent years, MPA research made several important advances but some questions still remain unresolved.

Key Concepts:

Marine protected areas are a useful management tool.

Marine protected areas can have ecological, fisheries and socio‐economic benefits.

Partial protection confers less ecological benefits than full protection.

Effects of marine protected areas mainly depend on their design and age, on the socio‐cultural context in which they are established and on the life history traits of the species targeted by protection.

Effective marine protected areas need to be well enforced.

The global coverage of marine protected areas is still very low.
Diet, Changes in Gene Expression and Human Evolution
Authors: Luca Francesca 
Published: April 2013

AbstractChanges in food availability and diet represent selective pressures that acted on multiple biological processes and anatomical features during human evolution. Anthropological studies have long investigated these dietary transitions; however, many questions are still open and aspects of these events are still strongly debated. More recently, evolutionary geneticists have provided evidence, both genome‐wide and from single‐gene studies, that diet is an important evolutionary force in humans. Changes in regulation of gene expression have played a major role during human evolution in response to a variety of selective pressures including dietary transitions. Furthermore, recent studies have highlighted the role of variation in gene regulation in risk for common diseases. Future studies promise to leverage the information from variation in gene expression to learn about adaptations to dietary shifts and disease predisposition in humans.Key Concepts:Changes in food availability and diet composition during hominin evolution created strong selective pressures on multiple biological processes and anatomical features.Genes involved in metabolism carry a signature of selection in single‐gene and genome‐wide studies.The two most interpretable examples of genetic adaptations to dietary shifts in humans have implied changes in the expression level of the lactase and amylase genes.Adaptations to dietary changes may have acted on different molecular aspects of regulation of gene expression.By gaining further knowledge on past human diets, it is possible to achieve a better understanding of potential adaptations to and clinical consequences of our current ones.
Biological/Biochemical Features and Molecular Genetics of Specific Language Impairment (
SLI
)
Authors: Caylak Emrah 
Published: April 2013

Abstract

Common learning disorders include attention‐deficit hyperactivity disorder, dyslexia, specific language impairment (SLI), speech–sound disorder and dyspraxia. They are influenced by genes and several research groups to attempt to identify susceptibility genes of learning disorders through the sequential analysis of genetic linkage and association. This review highlights the genetic contribution to SLI and the current molecular genetic researches aimed at identifying susceptibility and candidate genes for SLI. Currently, four susceptibility loci and three candidate genes (
CMIP
,
ATP2C2
and
CNTNAP2
) associated with SLI have been found. This review also summarises the biological/biochemical features of SLI. The success of dietary intervention of nutritional supplements (i.e. thiamine and some fatty acids) to improve learning abilities in SLI and dyslexia suggests that a greater understanding of biochemical abnormalities may provide a useful addition with other treatment procedures for these learning disorders.

Key Concepts:

Learning disorders may cause the learner to receive and process some information inaccurately. People with learning disorders may have problems of basic psychological processes involved in understanding or in using language, spoken or written, that may manifest itself in an imperfect ability to listen, think, speak, read, write, spell or do mathematical calculations.

Individuals with specific language impairment (SLI) seem to have problems in pragmatics, such as discourse maintenance, use and range of speech acts and narrative abilities.

Genetic factors are important in specific language impairment.

Molecular genetic researches should be aimed to identify susceptibility genes for SLI.

Molecular advances in SLI will help to set the research agendas for future studies to follow.

The association and linkage studies of learning disorders may help us to understand the biological basis of normal learning variation, and shed light on more fundamental questions regarding the origin of human speech and language.
Lipid Rafts
Authors: Germain Véronique , Perraki Artemis , Mongrand Sébastien 
Published: April 2013

Abstract

The knowledge about the structure of the biological membrane changed during the last 70 years. In the 70s, Singer and Nicholson proposed the fluid mosaic model, a major conceptual breakthrough in which amphiphilic proteins reside within the lipid bilayer. In this dynamic structure, components can move laterally. Further works led to major modifications of this model. Indeed, functional aspects of trafficking and signal transduction suggested that lipids and proteins do not distribute randomly but can be sequestered in small domains, thus enhancing protein–protein interactions and speeding up signal transduction and enzyme activity. The ‘raft hypothesis’ was born. Rafts are small and transient microdomains enriched in sphingolipids and sterols, together with specific proteins with important functions. This hypothesis explains the heterogeneity of the distribution of membrane proteins by a spontaneous demixing of lipids to form domains involved in signal transduction, cell trafficking and host–pathogen relationship.

Key Concepts:

Biological membranes are organised in small, dynamic and transient domains called lipid rafts.

Lipid rafts exist in all eukaryotic cells, mostly in the plasma membrane.

Lipid rafts are enriched in sphingolipids and sterols, and depleted in phosphoglycerolipids.

Lipid rafts are involved in signal transduction pathways, cell trafficking and host–pathogen relationship.
Potassium in Plants
Authors: Amtmann Anna , Rubio Francisco 
Published: April 2013

Abstract

Potassium (K) is an essential macronutrient for plants involved in many physiological processes. It is important for crop yield as well as for the quality of edible parts of crops, as it is also required in human nutrition. Although K is not assimilated into organic matter, K deficiency has a strong impact on plant metabolism. Plant responses to low K involve changes in the concentrations of many metabolites as well as alteration in the transcriptional levels of many genes and in the activity of many enzymes. Today, these changes can be studied with high throughput technologies that allow a quantitative description of metabolic responses to K deprivation at multiple levels. To ensure K nutrition, plant roots are endowed with high‐ and low‐affinity uptake systems, some of which have been identified and characterised over the last decades of research.

Key Concepts:

K is an essential macronutrient required for plant growth and development.

K deficiency affects many essential physiological and metabolic processes.

The K status determines the profile and distribution of primary metabolites in plant tissues.

K nutrition is closely related to sugar allocation, nitrogen assimilation and amino acid levels.

High‐throughput technologies allow researchers to determine simultaneously a large number of metabolites, transcript levels and enzyme activities in response to K supply.

K deficiency leads to build‐up of sugars, down‐regulation of nitrate uptake and synthesis of nitrogen‐rich amino acids.

Roots are endowed with high‐ and low‐affinity K uptake systems that ensure K nutrition in a wide range of external concentrations.

hak5 transporters mediate high‐affinity K uptake and akt1 channels mediate low‐affinity K uptake.

Under certain conditions akt1 channels can also mediate K uptake from very low concentrations.

Additional unidentified systems may also promote root K uptake.
Evolution of Plant
Micro
RNAs
Authors: Tamas Dalmay 
Published: April 2013

Abstract

Microribonucleic acids (miRNAs)
are small noncoding regulatory molecules encoded in the genome and generated through several processing steps. They recognise specific messenger RNAs and regulate their expression by cleavage or by translational inhibition. MiRNAs were only discovered approximately 10 years ago but it quickly became evident that they play an important role in development and stress responses. Initially it was thought that all miRNAs are conserved in plants because the technology only allowed to sequence the most abundant miRNAs. However, the development of next generation sequencing technologies allowed researchers to generate millions of sequencing reads in a sample, which resulted in the identification of the less abundant miRNAs. Analysis of large‐scale sequencing data revealed that the number of nonconserved miRNAs is much larger than previously thought. This review focuses on the evolution of plant
MIRNA
genes from protein‐coding genes by describing the difference between conserved and nonconserved
MIRNA
families.

Key Concepts:

MicroRNAs are small noncoding regulatory molecules.

Primary miRNA transcripts are folded into a stem–loop secondary structure, which is cleaved twice by DICER‐LIKE1 releasing the microRNA duplex.

One strand of the microRNA duplex is incorporated into an ARGONAUTE complex and guides the complex to specific mRNAs.

The ARGONAUTE complex usually cleaves the target mRNA but it also suppresses the translation of noncleaved mRNAs.

Some
MIRNA
genes are ancient and conserved in all embryophytes but there are nonconserved
MIRNA
families that are only in angiosperms or specific to monocots or dicots. A large number of
MIRNA
families are even divergent between dicot families.

New
MIRNA
genes can potentially evolve from any inverted repeats but the most evidence exists for generation from inverse duplication of protein‐coding genes followed by deletions and mutations.

Indirect evidence suggests rapid birth and death of
MIRNA
genes: approximately 1–3
MIRNA
genes per million years in the
Arabidopsis
lineage.

Nonconserved
MIRNA
genes are weakly expressed, imprecisely processed, show uniform nucleotide divergence and many lack targets, suggesting that they are evolving neutrally.

Nonconserved
MIRNA
genes could be a source of ‘regulatory diversity’, which can be selected for if they acquire target genes and that is advantageous for the plant, maybe in a new environment.