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Cell
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Mar 28, 2013

Volume 153Issue 1p1-272
Open Archive
On the cover: The kind of food an organism consumes has a broad reaching impact on its development, behavior, and lifespan. In this issue, two papers, MacNeil et al. (pp. 240–252) and Watson et al. (pp. 253–266), explore the effects of diet on these life-history traits in the nematode C. elegans. Combining nutrigenomics and network analyses, they find that different diets affect traits via distinct mechanisms. The response to diet is coupled to metabolic changes, and disruptions of some of these specific metabolic pathways correspond to inborn errors of metabolism in humans. The cover features a “native-art-inspired abstraction” of a worm eating a bacterial diet and illustrates the interconnectedness between diet, nuclear gene regulatory networks, mitochondrial networks, and their effects on life-history traits such as development and brood size. Cover art by Lesley T. MacNeil....
On the cover: The kind of food an organism consumes has a broad reaching impact on its development, behavior, and lifespan. In this issue, two papers, MacNeil et al. (pp. 240–252) and Watson et al. (pp. 253–266), explore the effects of diet on these life-history traits in the nematode C. elegans. Combining nutrigenomics and network analyses, they find that different diets affect traits via distinct mechanisms. The response to diet is coupled to metabolic changes, and disruptions of some of these specific metabolic pathways correspond to inborn errors of metabolism in humans. The cover features a “native-art-inspired abstraction” of a worm eating a bacterial diet and illustrates the interconnectedness between diet, nuclear gene regulatory networks, mitochondrial networks, and their effects on life-history traits such as development and brood size. Cover art by Lesley T. MacNeil.

Leading Edge

In This Issue

Select

  • Linking Long Noncoding RNAs to Function

    Although the vast majority of the human genome is devoid of protein-coding capacity, we now know that amidst the “dark matter” are an estimated 10,000 to 200,000 long noncoding RNAs (lncRNAs). This Select highlights recent insights into the regulation of lncRNAs' expression and their unique roles.

Voices

  • Noncoding RNAs and Cancer

    A decade after RNAi was found in mammals, clinical studies using microRNA antagonists and lipid-encapsulated siRNAs are showing promise for inhibiting hepatitis C virus replication and knocking down genes in the liver. The biggest challenge to RNA-based cancer therapeutics remains delivery into cells outside of the liver, which is critical for treating disseminated cancer. Attractive approaches to targeted delivery being developed avoid liposomes and use RNAs covalently linked to small-molecule conjugates or RNA aptamers.

Previews

  • Synovial Sarcoma Mechanisms: A Series of Unfortunate Events

    • Jesper Q. Svejstrup
    Human synovial sarcoma is caused by a chromosome translocation, which fuses DNA encoding SSX to that encoding the SS18 protein. Kadoch and Crabtree now show that the resulting cellular transformation stems from disruption of the normal architecture and function of the human SWI/SNF (BAF) complex.
  • Ring around the Ro-sie: RNA-Mediated Alterations of PNPase Activity

    • Brian J. Geiss,
    • Jeffrey Wilusz
    Chen et al. demonstrate a new way by which noncoding RNAs tailor the function of multicomponent complexes. They show that a noncoding RNA interacts with an exoribonuclease, altering its substrate specificity and enzymatic activity by serving as a ribonucleoprotein scaffold and, perhaps, a gate for entry of the RNA substrate.
  • Cullins Getting Undressed by the Protein Exchange Factor Cand1

    • Michael H. Olma,
    • Ivan Dikic
    Cullin-RING ubiquitin ligase complexes (CRLs) rely on a vast array of adaptor proteins to recognize their substrates. Pierce et al. and related papers from Zemla et al. and Wu et al. in Nature Communications show that Cand1 promotes exchange of adaptor proteins to regulate the CRL repertoire.

Reviews

  • Lessons from the Cancer Genome

    • Levi A. Garraway,
    • Eric S. Lander
    Systematic studies of the cancer genome have exploded in recent years. These studies have revealed scores of new cancer genes, including many in processes not previously known to be causal targets in cancer. The genes affect cell signaling, chromatin, and epigenomic regulation; RNA splicing; protein homeostasis; metabolism; and lineage maturation. Still, cancer genomics is in its infancy. Much work remains to complete the mutational catalog in primary tumors and across the natural history of cancer, to connect recurrent genomic alterations to altered pathways and acquired cellular vulnerabilities, and to use this information to guide the development and application of therapies.
  • Interplay between the Cancer Genome and Epigenome

    • Hui Shen,
    • Peter W. Laird
    Cancer arises as a consequence of cumulative disruptions to cellular growth control with Darwinian selection for those heritable changes that provide the greatest clonal advantage. These traits can be acquired and stably maintained by either genetic or epigenetic means. Here, we explore the ways in which alterations in the genome and epigenome influence each other and cooperate to promote oncogenic transformation. Disruption of epigenomic control is pervasive in malignancy and can be classified as an enabling characteristic of cancer cells, akin to genome instability and mutation.
  • Influence of Metabolism on Epigenetics and Disease

    • William G. Kaelin Jr.,
    • Steven L. McKnight
    Chemical modifications of histones and DNA, such as histone methylation, histone acetylation, and DNA methylation, play critical roles in epigenetic gene regulation. Many of the enzymes that add or remove such chemical modifications are known, or might be suspected, to be sensitive to changes in intracellular metabolism. This knowledge provides a conceptual foundation for understanding how mutations in the metabolic enzymes SDH, FH, and IDH can result in cancer and, more broadly, for how alterations in metabolism and nutrition might contribute to disease.

Articles

Erratum

SnapShot

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