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<jats:p>Dust deposition in the Southern Ocean constitutes a critical modulator of past global climate variability, but how it has varied temporally and geographically is underdetermined. Here, we present data sets of glacial-interglacial dust-supply cycles from the largest Southern Ocean sector, the polar South Pacific, indicating three times higher dust deposition during glacial periods than during interglacials for the past million years. Although the most likely dust source for the South Pacific is Australia and New Zealand, the glacial-interglacial pattern and timing of lithogenic sediment deposition is similar to dust records from Antarctica and the South Atlantic dominated by Patagonian sources. These similarities imply large-scale common climate forcings, such as latitudinal shifts of the southern westerlies and regionally enhanced glaciogenic dust mobilization in New Zealand and Patagonia.</jats:p>

<jats:p> Plant cells are immobile; thus, plant growth and development depend on cell expansion rather than cell migration. The molecular mechanism by which the plasma membrane initiates changes in the cell expansion rate remains elusive. We found that a secreted peptide, RALF (rapid alkalinization factor), suppresses cell elongation of the primary root by activating the cell surface receptor FERONIA in <jats:italic>Arabidopsis thaliana</jats:italic> . A direct peptide-receptor interaction is supported by specific binding of RALF to FERONIA and reduced binding and insensitivity to RALF-induced growth inhibition in <jats:italic>feronia</jats:italic> mutants. Phosphoproteome measurements demonstrate that the RALF-FERONIA interaction causes phosphorylation of plasma membrane H <jats:sup>+</jats:sup> –adenosine triphosphatase 2 at Ser <jats:sup>899</jats:sup> , mediating the inhibition of proton transport. The results reveal a molecular mechanism for RALF-induced extracellular alkalinization and a signaling pathway that regulates cell expansion. </jats:p>

<jats:p> One of the most complex eyes in the animal kingdom can be found in species of stomatopod crustaceans (mantis shrimp), some of which have 12 different photoreceptor types, each sampling a narrow set of wavelengths ranging from deep ultraviolet to far red (300 to 720 nanometers) ( <jats:italic>1</jats:italic> – <jats:italic>3</jats:italic> ). Functionally, this chromatic complexity has presented a mystery ( <jats:italic>3</jats:italic> – <jats:italic>5</jats:italic> ). Why use 12 color channels when three or four are sufficient for fine color discrimination? Behavioral wavelength discrimination tests (Δλ functions) in stomatopods revealed a surprisingly poor performance, ruling out color vision that makes use of the conventional color-opponent coding system ( <jats:italic>6</jats:italic> – <jats:italic>8</jats:italic> ). Instead, our experiments suggest that stomatopods use a previously unknown color vision system based on temporal signaling combined with scanning eye movements, enabling a type of color recognition rather than discrimination. </jats:p>

<jats:p> Animal displays are often perceived by intended and unintended receivers in more than one sensory system. In addition, cues that are an incidental consequence of signal production can also be perceived by different receivers, even when the receivers use different sensory systems to perceive them. Here we show that the vocal responses of male túngara frogs ( <jats:italic>Physalaemus pustulosus</jats:italic> ) increase twofold when call-induced water ripples are added to the acoustic component of a rival’s call. Hunting bats ( <jats:italic>Trachops cirrhosus</jats:italic> ) can echolocate this signal by-product and prefer to attack model frogs when ripples are added to the acoustic component of the call. This study illustrates how the perception of a signal by-product by intended and unintended receivers through different sensory systems generates both costs and benefits for the signaler. </jats:p>

<jats:p>Liver regeneration requires spatially and temporally precisely coordinated proliferation of the two major hepatic cell populations, hepatocytes and liver sinusoidal endothelial cells (LSECs), to reconstitute liver structure and function. The underlying mechanisms of this complex molecular cross-talk remain elusive. Here, we show that the expression of Angiopoietin-2 (Ang2) in LSECs is dynamically regulated after partial hepatectomy. During the early inductive phase of liver regeneration, Ang2 down-regulation leads to reduced LSEC transforming growth factor–β1 production, enabling hepatocyte proliferation by releasing an angiocrine proliferative brake. During the later angiogenic phase of liver regeneration, recovery of endothelial Ang2 expression enables regenerative angiogenesis by controlling LSEC vascular endothelial growth factor receptor 2 expression. The data establish LSECs as a dynamic rheostat of liver regeneration, spatiotemporally orchestrating hepatocyte and LSEC proliferation through angiocrine- and autocrine-acting Ang2, respectively.</jats:p>

<jats:p>The physical manifestation of learning and memory formation in the brain can be expressed by strengthening or weakening of synaptic connections through morphological changes. Local actin remodeling underlies some forms of plasticity and may be facilitated by local β-actin synthesis, but dynamic information is lacking. In this work, we use single-molecule in situ hybridization to demonstrate that dendritic β-actin messenger RNA (mRNA) and ribosomes are in a masked, neuron-specific form. Chemically induced long-term potentiation prompts transient mRNA unmasking, which depends on factors active during synaptic activity. Ribosomes and single β-actin mRNA motility increase after stimulation, indicative of release from complexes. Hence, the single-molecule assays we developed allow for the quantification of activity-induced unmasking and availability for active translation. Further, our work demonstrates that β-actin mRNA and ribosomes are in a masked state that is alleviated by stimulation.</jats:p>

<jats:p>The transcription and transport of messenger RNA (mRNA) are critical steps in regulating the spatial and temporal components of gene expression, but it has not been possible to observe the dynamics of endogenous mRNA in primary mammalian tissues. We have developed a transgenic mouse in which all β-actin mRNA is fluorescently labeled. We found that β-actin mRNA in primary fibroblasts localizes predominantly by diffusion and trapping as single mRNAs. In cultured neurons and acute brain slices, we found that multiple β-actin mRNAs can assemble together, travel by active transport, and disassemble upon depolarization by potassium chloride. Imaging of brain slices revealed immediate early induction of β-actin transcription after depolarization. Studying endogenous mRNA in live mouse tissues provides insight into its dynamic regulation within the context of the cellular and tissue microenvironment.</jats:p>

<jats:p> Three iron-sulfur proteins–HydE, HydF, and HydG–play a key role in the synthesis of the [2Fe] <jats:sub>H</jats:sub> component of the catalytic H-cluster of FeFe hydrogenase. The radical <jats:italic>S</jats:italic> -adenosyl- <jats:sc>l</jats:sc> -methionine enzyme HydG lyses free tyrosine to produce <jats:italic>p</jats:italic> -cresol and the CO and CN <jats:sup>−</jats:sup> ligands of the [2Fe] <jats:sub>H</jats:sub> cluster. Here, we applied stopped-flow Fourier transform infrared and electron-nuclear double resonance spectroscopies to probe the formation of HydG-bound Fe-containing species bearing CO and CN <jats:sup>−</jats:sup> ligands with spectroscopic signatures that evolve on the 1- to 1000-second time scale. Through study of the <jats:sup>13</jats:sup> C, <jats:sup>15</jats:sup> N, and <jats:sup>57</jats:sup> Fe isotopologs of these intermediates and products, we identify the final HydG-bound species as an organometallic Fe(CO) <jats:sub>2</jats:sub> (CN) synthon that is ultimately transferred to apohydrogenase to form the [2Fe] <jats:sub>H</jats:sub> component of the H-cluster. </jats:p>

<jats:p>The progressive depletion of quiescent “bystander” CD4 T cells, which are nonpermissive to HIV infection, is a principal driver of the acquired immunodeficiency syndrome (AIDS). These cells undergo abortive infection characterized by the cytosolic accumulation of incomplete HIV reverse transcripts. These viral DNAs are sensed by an unidentified host sensor that triggers an innate immune response, leading to caspase-1 activation and pyroptosis. Using unbiased proteomic and targeted biochemical approaches, as well as two independent methods of lentiviral short hairpin RNA–mediated gene knockdown in primary CD4 T cells, we identify interferon-γ–inducible protein 16 (IFI16) as a host DNA sensor required for CD4 T cell death due to abortive HIV infection. These findings provide insights into a key host pathway that plays a central role in CD4 T cell depletion during disease progression to AIDS.</jats:p>

<jats:p>How the immune system adapts to malnutrition to sustain immunity at barrier surfaces, such as the intestine, remains unclear. Vitamin A deficiency is one of the most common micronutrient deficiencies and is associated with profound defects in adaptive immunity. Here, we found that type 3 innate lymphoid cells (ILC3s) are severely diminished in vitamin A–deficient settings, which results in compromised immunity to acute bacterial infection. However, vitamin A deprivation paradoxically resulted in dramatic expansion of interleukin-13 (IL-13)–producing ILC2s and resistance to nematode infection in mice, which revealed that ILCs are primary sensors of dietary stress. Further, these data indicate that, during malnutrition, a switch to innate type 2 immunity may represent a powerful adaptation of the immune system to promote host survival in the face of ongoing barrier challenges.</jats:p>