Catálogo de publicaciones - revistas

<jats:p> Highlights from the <jats:italic>Science</jats:italic> family of journals </jats:p>

<jats:p>Editors’ selections from the current scientific literature</jats:p>

<jats:title>A fishy tale of long and short life span</jats:title> <jats:p> Fish have wide variations in life span even within closely related species. One such example are the rockfish species found along North Pacific coasts, which have life spans ranging from 11 to more than 200 years. Kolora <jats:italic>et al</jats:italic> . sequenced and performed a genomic analysis of 88 rockfish species, including long-read sequencing of the genomes of six species (see the Perspective by Lu <jats:italic>et al</jats:italic> .). From this analysis, the authors unmasked the genetic drivers of longevity evolution, including immunity and DNA repair–related pathways. Copy number expansion in the butyrophilin gene family was shown to be positively associated with life span, and population historical dynamics and life histories correlated differently between long- and short-lived species. These results support the idea that inflammation may modulate the aging process in these fish. —LMZ </jats:p>

<jats:title>Fibril motion improves peptide signaling</jats:title> <jats:p> Artificial scaffolds that bear the peptide-signaling sequences of proteins for tissue regeneration often have limited effectiveness. Álvarez <jats:italic>et al</jats:italic> . synthesized supramolecular peptide fibril scaffolds bearing two peptide sequences that promote nerve regeneration, one that reduces glial scarring and another that promotes blood vessel formation (see the Perspective by Wojciechowski and Stevens). In a mouse model of paralyzing human spinal cord injury, mutations in a tetrapeptide domain outside of the signaling regions improved recovery by promoting intense supramolecular motion within the fibrils. The mutation with the most intense dynamics resulted in corticospinal axon regrowth and myelination, functional revascularization, and motor neuron survival. —PDS </jats:p>

<jats:title>Where and when of memory consolidation</jats:title> <jats:p> Episodic memory is initially encoded in the hippocampus and later transferred to other brain regions for long-term storage. Synaptic plasticity underlies learning and plays a critical role in memory consolidation. However, it remains largely unknown where and when synaptic plasticity occurs and how it shapes the neuronal representation. Goto <jats:italic>et al</jats:italic> . developed a new tool for controlling early structural long-term potentiation (sLTP). By selectively manipulating sLTP, the authors showed that the local circuitry in hippocampal area CA1 is required for memory formation shortly after the encoding event. The local circuitry is also important for offline memory consolidation within 24 hours. The anterior cingulate cortex, another brain region directly connected with area CA1, is crucial for memory consolidation during sleep on the second night. —PRS </jats:p>

<jats:title>Resolution of the σ-hole</jats:title> <jats:p> Anisotropic distribution of charges on atoms plays an important role in intermolecular interactions, yet direct experimental imaging remains a long-standing challenge. A good example is the σ-hole, an anisotropic charge distribution on a halogen atom covalently linked to carbon atoms. The σ-hole gives rise to the halogen-bonding mechanism, which is well known in supramolecular chemistry despite its existence being confirmed only indirectly. Mallada <jats:italic>et al</jats:italic> . developed Kelvin probe force microscopy with a specifically functionalized tip and report direct real-space visualization of the σ-hole, revealing its strong anisotropic charge distribution. The authors show that this technique, which relies entirely on electrostatic interactions, may be a powerful tool with which to study anisotropic atomic charge distributions. —YS </jats:p>

<jats:title>Autoimmunity in Lewy body dementia</jats:title> <jats:p> Lewy body dementia (LBD) is a brain disease that leads to progressive decline in thinking, movement, and independent function. It results from the build-up of microscopic deposits called Lewy bodies, which develop from the aggregation of a misfolded protein called α-synuclein. Gate <jats:italic>et al</jats:italic> . observed immune cells known as T cells in the brains of LBD patients (see the Perspective by Krot and Rolls). Genomics analysis revealed that T cells traffic to the LBD brain and are associated with neuronal damage. When stimulated with α-synuclein, LBD patient T cells secrete an inflammatory protein known to damage neurons. These findings suggest an unexpected detrimental role of the immune system in LBD. —SMH </jats:p>