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<jats:p> A monthly roundup of recent news and projects of <jats:italic>Science</jats:italic> 's publisher, the American Association for the Advancement of Science. </jats:p>

<jats:p>Epigenetic signals are responsible for the establishment, maintenance, and reversal of metastable transcriptional states that are fundamental for the cell’s ability to “remember” past events, such as changes in the external environment or developmental cues. Complex epigenetic states are orchestrated by several converging and reinforcing signals, including transcription factors, noncoding RNAs, DNA methylation, and histone modifications. Although all of these pathways modulate transcription from chromatin in vivo, the mechanisms by which epigenetic information is transmitted through cell division remain unclear. Because epigenetic states are metastable and change in response to the appropriate signals, a deeper understanding of their molecular framework will allow us to tackle the dysregulation of epigenetics in disease.</jats:p>

<jats:p>Transient populations of cis- and trans-acting small RNAs have recently emerged as key regulators of extensive epigenetic changes taking place during periconception, which encompasses gametogenesis, fertilization, and early zygotic development. These small RNAs are not only important to maintain genome integrity in the gametes and zygote, but they also actively contribute to assessing the compatibility of parental genomes at fertilization and to promoting long-term memory of the zygotic epigenetic landscape by affecting chromatin. Striking parallels exist in the biogenesis and modus operandi of these molecules among diverse taxa, unraveling universal themes of small-RNA–mediated epigenetic reprogramming during sexual reproduction.</jats:p>

<jats:p>Epigenetic modifications of the genome are generally stable in somatic cells of multicellular organisms. In germ cells and early embryos, however, epigenetic reprogramming occurs on a genome-wide scale, which includes demethylation of DNA and remodeling of histones and their modifications. The mechanisms of genome-wide erasure of DNA methylation, which involve modifications to 5-methylcytosine and DNA repair, are being unraveled. Epigenetic reprogramming has important roles in imprinting, the natural as well as experimental acquisition of totipotency and pluripotency, control of transposons, and epigenetic inheritance across generations. Small RNAs and the inheritance of histone marks may also contribute to epigenetic inheritance and reprogramming. Reprogramming occurs in flowering plants and in mammals, and the similarities and differences illuminate developmental and reproductive strategies.</jats:p>

<jats:p>Paramutation refers to the process by which homologous DNA sequences communicate in trans to establish meiotically heritable expression states. Although mechanisms are unknown, current data are consistent with the hypothesis that the establishment and heritable transmission of specific chromatin states underlies paramutation. Transcribed, noncoding tandem repeats and proteins implicated in RNA-directed transcriptional silencing in plants and yeast are required for paramutation, yet the specific molecules mediating heritable silencing remain to be determined.</jats:p>

<jats:p>Prions are an unusual form of epigenetics: Their stable inheritance and complex phenotypes come about through protein folding rather than nucleic acid–associated changes. With intimate ties to protein homeostasis and a remarkable sensitivity to stress, prions are a robust mechanism that links environmental extremes with the acquisition and inheritance of new traits.</jats:p>

<jats:p>Modeling videos suggest that around 4.4 million barrels of oil escaped from the broken Deepwater Horizon well.</jats:p>

<jats:title>Controlling Chloride Channels</jats:title> <jats:p> The CLC proteins are a large family of channels and transporters that transfer chloride ions across cell membranes. While structures of two prokaryotic CLCs have been determined, these do not include the cytoplasmic regulatory domains found in eukaryotic transporters, and the structures do not reveal the mechanism of Cl <jats:sup>−</jats:sup> /H <jats:sup>+</jats:sup> –coupled transport. <jats:bold> L. Feng <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="635" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1195230">635</jats:related-article> , published online 30 September; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6004" page="601" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1198306">Mindell</jats:related-article> </jats:bold> ) describe the structure of a eukaryotic CLC protein and found that the regulatory domains interacted closely with the transmembrane domain so that conformational changes are transmitted to the ion pathway. A gating glutamate in the eukaryote transporter is in a different conformation to prokaryotic structures, explaining the 2:1 stoichiometry of Cl <jats:sup>−</jats:sup> /H <jats:sup>+</jats:sup> exchange in eukaryotes. </jats:p>

<jats:title>Evolution, Gene Number, and Disease</jats:title> <jats:p> Slight variations in the numbers of copies of genes influence human disease and other characters. Variants can be hard to detect when they lie in heavily duplicated and widely similar regions of sequence known as “dark matter.” <jats:bold> Sudmant <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="641" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1197005">641</jats:related-article> ) have methods to tease apart the duplicated regions to reveal singly unique nucleotide identifiers. These have turned out to be among the most variable seen in different human population groups—most notably among genes for neurodevelopment and neurological diseases. Such polymorphisms can be genotyped with specificity and may help us understand how variation in copy number may affect human evolution and disease. </jats:p>