The Current Opinion journals were developed out of the recognition that it is increasingly difficult for specialists to keep up to date with the expanding volume of information published in their subject. Elsevier’s Current Opinion journals comprise of 26 leading titles in life sciences and adjacent fields.

Current Opinion in Genetics & Development

5-Year Impact Factor: 5.934
Issues per year: 6 issues
Editorial Board

Current Opinion in Genetics & Development

Current Opinion in Genetics and Development aims to stimulate scientifically grounded, interdisciplinary, multi-scale debate and exchange of ideas. It contains polished, concise and timely reviews and opinions, with particular emphasis on those articles published in the past two years. In addition to describing recent trends, the authors are encouraged to give their subjective opinion of the topics discussed.

In Current Opinion in Genetics and Development we help the reader by providing in a systematic manner:

1. The views of experts on current advances in their field in a clear and readable form.
2. Evaluations of the most interesting papers, annotated by experts, from the great wealth of original publications

Current Opinion in Genetics and Development will serve as an invaluable source of information for researchers, lecturers, teachers, professionals, policy makers and students.

Division of the subject into sections
The subject of Genetics and Development is divided into six themed sections, each of which is reviewed once a year.

Genetic and cellular mechanisms of oncogenesis
Chromosomes, genomes and expression mechanisms
Molecular and genetic bases of disease
Developmental mechanisms, patterning and evolution
Differentiation and gene regulation
Genetics of system biology

Selection of topics to be reviewed

Section Editors, who are major authorities in the field, are appointed by the Editors of the journal. They divide their section into a number of topics, ensuring that the field is comprehensively covered and that all issues of current importance are emphasised. Section Editors commission reviews from authorities on each topic that they have selected. The Editorial Board provides support to the Editors and the Section Editors with their comments and suggestions on names and topics.

Review articles in Current Opinion in Genetics and Development are by invitation only.

Review Articles

Authors write short review articles in which they present recent developments in their subject, emphasizing the aspects that, in their opinion, are most important. In addition, they provide short annotations to the papers that they consider to be most interesting from all those published in their topic over the previous two years.

Editorial Overview

Section Editors write a short overview at the beginning of the section to introduce the reviews and to draw the reader's attention to any particularly interesting developments.

This successful format has made Current Opinion in Genetics and Development one of the most highly regarded and highly cited review journals in the field (Impact factor = 8.987).

Best Cited over the last year.

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Active human retrotransposons: Variation and disease

Mobile DNAs, also known as transposons or 'jumping genes', are widespread in nature and comprise an estimated 45% of the human genome. Transposons are divided into two general classes based on their transposition intermediate (DNA or RNA). Only one subclass, the non-LTR retrotransposons, which includes the Long INterspersed Element-1 (LINE-1 or L1), is currently active in humans as indicated by 96 disease-causing insertions. The autonomous LINE-1 is capable of retrotransposing not only a copy…

Volume 22, Issue 3, 01 June 2012, Pp 191-203
Dustin C. Hancks | Haig H. Kazazian

Chromatin higher-order structures and gene regulation

Genomic DNA in the eukaryotic nucleus is hierarchically packaged by histones into chromatin to fit inside the nucleus. The dynamics of higher-order chromatin compaction play a crucial role in transcription and other biological processes inherent to DNA. Many factors, including histone variants, histone modifications, DNA methylation, and the binding of non-histone architectural proteins regulate the structure of chromatin. Although the structure of nucleosomes, the fundamental repeating unit of…

Volume 21, Issue 2, 01 April 2011, Pp 175-186
Guohong Li | Danny Reinberg

Genetic architecture in autism spectrum disorder

Autism spectrum disorder (ASD) is characterized by impairments in reciprocal social interaction and communication, and by restricted and repetitive behaviors. Family studies indicate a significant genetic basis for ASD susceptibility, and genomic scanning is beginning to elucidate the underlying genetic architecture. Some 5-15% of individuals with ASD have an identifiable genetic etiology corresponding to known chromosomal rearrangements or single gene disorders. Rare (<1% frequency) de novo or…

Volume 22, Issue 3, 01 June 2012, Pp 229-237
Bernie Devlin | Stephen W. Scherer

Cancer epigenomics: Beyond genomics

For many years cancer research has focused on genetic defects, but during the last decade epigenetic deregulation has been increasingly recognized as a hallmark of cancer. The advent of genome-scale analysis techniques, including the recently developed next-generation sequencing, has enabled an invaluable advance in the molecular mechanisms underlying tumor initiation, progression, and expansion. In this review we describe recent advances in the field of cancer epigenomics concerning DNA…

Volume 22, Issue 1, 01 February 2012, Pp 50-55
Juan Sandoval | Manel Esteller

Function and regulation of the Mediator complex

Over the past few years, advances in biochemical and genetic studies of the structure and function of the Mediator complex have shed new light on its subunit architecture and its mechanism of action in transcription by RNA polymerase II (pol II). The development of improved methods for reconstitution of recombinant Mediator subassemblies is enabling more in-depth analyses of basic features of the mechanisms by which Mediator interacts with and controls the activity of pol II and the general…

Volume 21, Issue 2, 01 April 2011, Pp 225-230
Ronald C. Conaway | Joan Weliky Conaway

MTOR in aging, metabolism, and cancer

The target of rapamycin (TOR) is a highly conserved serine/threonine kinase that is part of two structurally and functionally distinct complexes, TORC1 and TORC2. In multicellular organisms, TOR regulates cell growth and metabolism in response to nutrients, growth factors and cellular energy. Deregulation of TOR signaling alters whole body metabolism and causes age-related disease. This review describes the most recent advances in TOR signaling with a particular focus on mammalian TOR (mTOR) in…

Volume 23, Issue 1, 01 February 2013, Pp 53-62
Marion Cornu | Verena Albert | Michael N. Hall

MiRNA profiling of cancer

A steadily growing number of studies have shown that microRNAs have key roles in the regulation of cellular processes and that their dysregulation is essential to keep the malignant phenotype of cancer cells. The distorted and unique expression profile of microRNAs in different types and subsets of tumor coupled with their presence in biological fluids make of microRNAs an attractive source of sensitive biomarkers. Here, we will discuss how microRNA profiles are altered in cancer, highlighting…

Volume 23, Issue 1, 01 February 2013, Pp 3-11
Gianpiero Di Leva | Carlo M. Croce

Cellular senescence: Putting the paradoxes in perspective

Cellular senescence arrests the proliferation of potential cancer cells, and so is a potent tumor suppressive mechanism, akin to apoptosis. Or is it? Why did cells evolve an anti-cancer mechanism that arrests, rather than kills, would-be tumor cells? Recent discoveries that senescent cells secrete growth factors, proteases and cytokines provide a shifting view-from senescence as a cell autonomous suppressor of tumorigenesis to senescence as a means to mobilize the systemic and local tissue…

Volume 21, Issue 1, 01 February 2011, Pp 107-112
Judith Campisi

Mechanisms for recurrent and complex human genomic rearrangements

During the last two decades, the importance of human genome copy number variation (CNV) in disease has become widely recognized. However, much is not understood about underlying mechanisms. We show how, although model organism research guides molecular understanding, important insights are gained from study of the wealth of information available in the clinic. We describe progress in explaining nonallelic homologous recombination (NAHR), a major cause of copy number change occurring when…

Volume 22, Issue 3, 01 June 2012, Pp 211-220
Pengfei Liu | Claudia M B Carvalho | P. J. Hastings | James R. Lupski

MicroRNAs and developmental timing

MicroRNAs regulate temporal transitions in gene expression associated with cell fate progression and differentiation throughout animal development. Genetic analysis of developmental timing in the nematode Caenorhabditis elegans identified two evolutionarily conserved microRNAs, lin-4/mir-125 and let-7, that regulate cell fate progression and differentiation in C. elegans cell lineages. MicroRNAs perform analogous developmental timing functions in other animals, including mammals. By regulating…

Volume 21, Issue 4, 01 August 2011, Pp 511-517
Victor Ambros

Combinatorial complexity in chromatin structure and function: Revisiting the histone code

Covalent modifications of histone proteins play key roles in transcription, DNA repair, recombination, and other such processes. Over a hundred histone modifications have been described, and a popular idea in the field is that the function of a single histone mark cannot be understood without understanding its combinatorial co-occurrence with other marks, an idea generally called the 'histone code hypothesis.' This idea is hotly debated, with increasing biochemical evidence for chromatin…

Volume 22, Issue 2, 01 April 2012, Pp 148-155
Oliver J. Rando

Hypoxia and energetic tumour metabolism

The hypoxia-inducible factor (HIF-1), in addition to genetic and epigenetic changes, is largely responsible for alterations in cell metabolism in hypoxic tumour cells. This transcription factor not only favours cell proliferation through the metabolic shift from oxidative phosphorylation to glycolysis and lactic acid production but also stimulates nutrient supply by mediating adaptive survival mechanisms. These include epithelial-mesenchymal transition, angiogenesis, autophagy, and synthesis…

Volume 21, Issue 1, 01 February 2011, Pp 67-72
M. Christiane Brahimi-Horn | Gregory Bellot | Jacques Pouysségur

Autophagy in tumorigenesis and energy metabolism: Friend by day, foe by night

Autophagy is the mechanism by which cells consume parts of themselves to survive starvation and stress. This self-cannibalization limits cell death and tissue inflammation, recycles energy and biosynthetic substrates and removes damaged proteins and organelles, accumulation of which is toxic. In normal tissues, autophagy-mediated damage mitigation may suppress tumorigenesis, while in advanced tumors macromolecular recycling may support survival by buffering metabolic demand under stress. As a…

Volume 21, Issue 1, 01 February 2011, Pp 113-119
Robin Mathew | Eileen White

Apoptosis and oncogenesis: Give and take in the BCL-2 family

The mitochondrial pathway of apoptosis constitutes one of the main safeguards against tumorigenesis. The BCL-2 family includes the central players of this pathway that regulate cell fate through the control of mitochondrial outer membrane permeabilization (MOMP), and important progress has been made in understanding the dynamic interactions between pro-apoptotic and anti-apoptotic BCL-2 proteins. In particular, recent studies have delineated a stepwise model for the induction of MOMP. BCL-2…

Volume 21, Issue 1, 01 February 2011, Pp 12-20
Fabien Llambi | Douglas R. Green

Cohesin: Genomic insights into controlling gene transcription and development

Over the past decade it has emerged that the cohesin protein complex, which functions in sister chromatid cohesion, chromosome segregation, and DNA repair, also regulates gene expression and development. Even minor changes in cohesin activity alter several aspects of development. Genome-wide analysis indicates that cohesin directly regulates transcription of genes involved in cell proliferation, pluripotency, and differentiation through multiple mechanisms. These mechanisms are poorly…

Volume 21, Issue 2, 01 April 2011, Pp 199-206
Dale Dorsett

Dystroglycanopathies: Coming into focus

A common group of muscular dystrophies is associated with the aberrant glycosylation of α-dystroglycan. These clinically heterogeneous disorders, collectively termed dystroglycanopathies, are often associated with central nervous system and more rarely eye pathology. Defects in a total of eight putative and demonstrated glycosyltransferases or accessory proteins of glycosyltransferases have been shown to cause a dystroglycanopathy phenotype. In recent years the systematic analysis of large…

Volume 21, Issue 3, 01 June 2011, Pp 278-285
Caroline Godfrey | A. Reghan Foley | Emma Clement | Francesco Muntoni

Chromatin states in pluripotent, differentiated, and reprogrammed cells

The pluripotent state of embryonic stem cells is maintained by a core network of transcription factors, and by chromatin remodelling factors that support an environment permissive for transcription. Polycomb and trithorax Group proteins enable 'bivalent' chromatin to be established at lineage-specific genes within pluripotent cells that is thought to poise genes for rapid activation upon induction of differentiation. As differentiation proceeds, chromatin condenses and there is a genome-wide…

Volume 21, Issue 2, 01 April 2011, Pp 140-146
Cynthia L. Fisher | Amanda G. Fisher

Existence and consequences of G-quadruplex structures in DNA

While the discovery of B-form DNA 60 years ago has defined our molecular view of the genetic code, other postulated DNA secondary structures, such as A-DNA, Z-DNA, H-DNA, cruciform and slipped structures have provoked consideration of DNA as a more dynamic structure. Four-stranded G-quadruplex DNA does not use Watson-Crick base pairing and has been subject of considerable speculation and investigation during the past decade, particularly with regard to its potential relevance to genome…

Volume 25, Issue 1, 01 April 2014, Pp 22-29
Pierre Murat | Shankar Balasubramanian

Switching TGFβ from a tumor suppressor to a tumor promoter

TGFβ acts as a potent tumor suppressor and tumor promoter in a context dependent manner. Tumor suppressive functions include inhibition of cell proliferation, induction of apoptosis and regulation of autophagy. As tumors develop they switch their response to TGFβ and utilise this factor as a potent promoter of cell motility, invasion, metastasis and tumor stem cell maintenance. These multifactorial tumor influencing actions of TGFβ involve regulation of an increasing number of signal…

Volume 21, Issue 1, 01 February 2011, Pp 93-99
Gareth J. Inman

Protein kinase signaling networks in cancer

Protein kinases orchestrate the activation of signaling cascades in response to extracellular and intracellular stimuli to control cell growth, proliferation, and survival. The complexity of numerous intracellular signaling pathways is highlighted by the number of kinases encoded by the human genome (539) and the plethora of phosphorylation sites identified in phosphoproteomic studies. Perturbation of these signaling networks by mutations or abnormal protein expression underlies the cause of…

Volume 21, Issue 1, 01 February 2011, Pp 4-11
John Brognard | Tony Hunter

RNA structure and the mechanisms of alternative splicing

Alternative splicing is a widespread means of increasing protein diversity and regulating gene expression in eukaryotes. Much progress has been made in understanding the proteins involved in regulating alternative splicing, the sequences they bind to, and how these interactions lead to changes in splicing patterns. However, several recent studies have identified other players involved in regulating alternative splicing. A major theme emerging from these studies is that RNA secondary structures…

Volume 21, Issue 4, 01 August 2011, Pp 373-379
C. Joel McManus | Brenton R. Graveley

Enhancer and promoter interactions-long distance calls

In metazoans, enhancers of gene transcription must often exert their effects over tens of kilobases of DNA. Over the past decade it has become clear that to do this, enhancers come into close proximity with target promoters with the looping away of intervening sequences. In a few cases proteins that are involved in the establishment or maintenance of these loops have been revealed but how the proper gene target is selected remains mysterious. Chromatin insulators had been appreciated as…

Volume 22, Issue 2, 01 April 2012, Pp 79-85
Ivan Krivega | Ann Dean

Phenotypic spectrum of the tubulin-related disorders and functional implications of disease-causing mutations

A spectrum of neurological disorders characterized by abnormal neuronal migration, differentiation, and axon guidance and maintenance have recently been attributed to missense and splice-site mutations in the genes that encode α-tubulin and β-tubulin isotypes TUBA1A, TUBA8, TUBB2B, and TUBB3, all of which putatively coassemble into neuronal microtubules. The resulting nervous system malformations can include different types of cortical malformations, defects in commissural fiber tracts, and…

Volume 21, Issue 3, 01 June 2011, Pp 286-294
Max A. Tischfield | Gustav Y. Cederquist | Mohan L. Gupta | Elizabeth C. Engle

MicroRNAs in neurons: Manifold regulatory roles at the synapse

The regulation of synapse formation and plasticity in the developing and adult brain underlies a complex interplay of intrinsic genetic programs and extrinsic factors. Recent research identified microRNAs (miRNAs), a class of small non-coding RNAs, as a new functional layer in this regulatory network. Within only a few years, a network of synaptic miRNAs and their target genes has been extensively characterized, highlighting the importance of this mechanism for synapse development and…

Volume 21, Issue 4, 01 August 2011, Pp 491-497
Gabriele Siegel | Reuben Saba | Gerhard Schratt

Vessel abnormalization: Another hallmark of cancer?. Molecular mechanisms and therapeutic implications

As a result of excessive production of angiogenic molecules, tumor vessels become abnormal in structure and function. By impairing oxygen delivery, abnormal vessels fuel a vicious cycle of non-productive angiogenesis, which creates a hostile microenvironment from where tumor cells escape through leaky vessels and which renders tumors less responsive to chemoradiation. While anti-angiogenic strategies focused on inhibiting new vessel growth and destroying pre-existing vessels, clinical studies…

Volume 21, Issue 1, 01 February 2011, Pp 73-79
Katrien De Bock | Sandra Cauwenberghs | Peter Carmeliet