<p>by Yacine Ben Chehida, Eva S. M. van der Heijden, Edward Page, Patricio A. Salazar C, Neil Rosser, Kimberly Gabriela Gavilanes Córdova, Mónica Sánchez-Prado, María José Sánchez-Carvajal, Franz Chandi, Alex P. Arias-Cruz, Maya Radford, Gerardo Lamas, Chris D. Jiggins, James Mallet, Melanie McClure, Camilo Salazar, Marianne Elias, Caroline N. Bacquet, Nicola J. Nadeau, Kanchon K. Dasmahapatra, Joana I. Meier</p>
Convergent evolution, the repeated evolution of similar phenotypes, is widespread in nature, but there are few studies investigating the genetic mechanisms of convergence across wide evolutionary timescales. The extent to which the same genetic mechanisms contribute to convergent evolution could reveal whether the pathway towards these fitness optima is flexible or constrained to follow a particular route, informing us about the predictability of evolution. Wing color pattern mimicry in Lepidoptera is a well-known example of convergent evolution, but as studies are restricted to a few closely related species, it is difficult to make general inferences about the predictability of evolution in this system. Here we study convergent evolution in multiple mimetic neotropical lepidopteran lineages that diverged between ~1 and 120 Mya, including seven species of Ithomiini and <i>Heliconius</i> butterflies and a day-flying <i>Chetone</i> moth. Across butterfly lineages that diverged up to ~30 Mya, the genetic variants most strongly associated with convergent color pattern switches are located in similar noncoding regions near the genes <i>ivory</i> and <i>optix</i>. In the more distantly related moth species, color pattern variation is associated with a ~1 Mb inversion which also contains <i>ivory</i>, closely mirroring the supergene architecture of the co-mimetic butterfly <i>Heliconius numata</i>. In contrast to previous studies on <i>Heliconius</i> butterflies, we find limited evidence that convergence among closely related Ithomiini species results from all…
Science Journals
<p>by Julia Penndorf, Brendan J. Barrett, Sonja Wild, John M. Martin, Lucy M. Aplin</p>
There is extensive evidence that the spread of innovation via social learning can facilitate uptake of new foraging behaviours in populations. In comparison, social learning about novel food types has received comparatively little attention. Yet the adoption of novel food is vital to persistence in, or colonisation of, novel environments. Here, we present a novel food (almonds in the shell, coloured either blue or red) in a two-option and control cultural diffusion experiment to five neighbouring roosts of 705 individually-marked sulphur-crested cockatoos (<i>Cacatua galerita</i>) living in a highly urbanised environment. From 4 initially trained individuals, a total of 349 individuals across all roosts learned to feed on the novel food within 10 days of first exposure. Using network-based diffusion-analysis (<i>N</i> = 214 learners out of 322 individuals with available social information), we demonstrated that this spread occurred almost exclusively through social learning, with information spreading through social network ties. Second, using experience-weighted attraction models, we described age-differences in social learning strategies, with juveniles, but not adults, exhibiting a conformist bias to prefer the most frequently chosen food colour. Third, when analysing 539 opening techniques of the novel food by 147 individuals across the five roosts, we found that opening techniques were more similar between roost communities when the distance between sites was small, or the degree of movement between sites was high. In addition, when focusing on a subset for which social association data were available (273 openings by 78 individuals), techniques tended to be more similar between close associates. Taken together, our study suggests that the adoption of novel food in urban-living sulphur-crested cockatoos is facilitated by social transmission of knowledge through networks,…
<p>by Aleksandra Otwinowska, Janusz Koszucki, Vyshakh R. Panicker, Jade Leconte, Sebastian Olejniczak, Kathryn E. Holt, Edward J. Feil, Eduardo P. C. Rocha, Bogna Smug, Barbara Maciejewska, Zuzanna Drulis-Kawa, Rafal J. Mostowy</p>
Virulent bacteriophages infecting <i>Klebsiella pneumoniae often show capsule-driven host tropism</i> due to the presence of capsule-specific depolymerases. Yet for temperate phages the genetic and functional basis of such capsular specificity remains less well understood. Depolymerases appear unexpectedly rare in prophage genomes, raising unresolved questions about which prophage genes mediate capsular specificity, whether this apparent scarcity reflects biological or ecological differences versus annotation limitation, and whether prophage-encoded receptor-binding proteins (RBPs) are functionally active. To address these questions, we analysed 3,900 <i>Klebsiella</i> genomes from diverse ecological niches to identify prophage-encoded proteins mediating capsular specificity. We conducted a genome-wide association study (GWAS) correlating prophage protein clusters (from 8,105 prophages) with confidently assigned bacterial K-loci. GWAS revealed statistically supported predictors of capsular specificity for 16 of the 35 most diverse K-loci analysed. These predictors were dominated by diverse RBPs, including classical β-helix depolymerases (6 predictors), SGNH-domain hydrolases predicted to deacetylate polysaccharides (6 predictors), and structurally novel RBPs lacking known depolymerase folds (2 predictors). Nearly one-third of K-loci yielded no statistically significant predictors. A targeted experimental screen of 50 candidate prophage depolymerases showed that 34 failed to yield detectable recombinant expression, and neither sequence similarity, structural prediction, nor prophage genomic context reliably predicted activity. Of the 14 active enzymes, 5 targeted a K-type different from that predicted of their bacterial host, and enzym…
<p>by Marc Talló-Parra, Mireia Puig-Torrents, Gemma Pérez-Vilaró, Sol Ribó Pons, Juana Díez</p>
Arboviruses induce acute lytic infection in human cells but establish persistent infection in their mosquito vectors, a viral strategy that is essential for sustained viral transmission. How mosquito cells maintain continuous production of viral progeny without compromising host cell viability remains a fundamental unresolved question. Because arbovirus replication in human cells relies on viral takeover of the host translational machinery, we investigated how translation is regulated during persistent infection in mosquito cells using chikungunya virus (CHIKV) as a model. A temporal analysis of viral RNA translation in RNAi-competent and RNAi-deficient <i>Aedes albopictus</i> cells revealed that persistence was associated with reduced viral protein production resulting from translation repression of viral RNAs. Subcellular localization analyses of the viral protein nsP2 and LC-MS/MS analyses of host tRNAs showed that, in contrast to human cells, CHIKV infection in mosquito cells neither induced nuclear relocalization of viral nsP2 to induce global host mRNA depletion, nor reshaped the tRNA modification landscape to compensate for the suboptimal codon usage of viral RNAs. Together, our results indicate that persistent infection in mosquito cells is characterized by a balanced host–virus translational state, in which limited viral translation is maintained while viral takeover of the host translational machinery is avoided. Notably, translation repression of viral RNAs was also observed during Zika virus (ZIKV) infection, suggesting that this mechanism may represent a general RNAi-independent feature of arbovirus persistence in mosquito cells.
<p>by Jian Guan, Rebecca Lee Hurto, Akash Rai, Janakraj Bhattrai, Christopher A. Azaldegui, Luis A. Ortiz-Rodríguez, Quancheng Liu, Julie S. Biteen, Lydia Freddolino, Ursula Jakob</p>
Uncovering what drives select biomolecules to form phase-separated condensates in vivo and identifying their physiological significance are topics of fundamental importance. Here, we show that nitrogen-starved <i>Escherichia coli</i> produces long-chain polyphosphates, which scaffold the RNA chaperone Hfq into high molecular weight complexes, which eventually phase separate together with components of the RNA translation and processing machinery. The presence of polyphosphate within these condensates controls Hfq function by selectively stabilizing polyadenylated RNAs involved in transcription and protein translation and by promoting interactions with translation- and RNA-metabolism-associated proteins involved in de novo protein synthesis. Lack of polyphosphate significantly impairs condensate formation, increases cell death, and hinders recovery from N-starvation. In functional analogy, we demonstrate that polyP contributes specifically to the formation of Processing (P)-bodies in human cell lines, revealing that a single, highly conserved and ancestral polyanion serves as a modulator for functional phase-separated condensate formation across the tree of life.
<p>by Thomas A. Püschel, Rachel M. Hurwitz, Chris Venditti</p>
Humans exhibit a striking and near-universal population-level right-hand preference, an evolutionary singularity unmatched among primates. Despite its pervasiveness, the origins of this lateralization remain poorly understood. Here, we combine phylogenetic comparative methods with meta-analysis to investigate manual lateralization across 41 anthropoid species (<i>n</i> = 2,025), testing longstanding eco-evolutionary hypotheses for handedness direction (mean handedness index, MHI) and strength (mean absolute handedness index, MABSHI). Our models reveal significant phylogenetic signal for both traits and identify <i>Homo sapiens</i> as an evolutionary outlier, exhibiting exceptional rightward bias and strength relative to phylogenetic expectations. However, this outlier status disappears when brain size (endocranial volume) and intermembral index are included, suggesting these factors are central to the emergence of human handedness. We also show that high MABSHI evolved early in hominin evolution, while MHI increased to unparalleled levels with the appearance of the genus <i>Homo</i>. Our findings identify bipedalism and neuroanatomical expansion as likely key drivers of uniquely human lateralization, while also revealing broader ecological patterns shaping handedness across primates. This work provides a framework for disentangling human-specific adaptations from general primate trends in the evolution of behavioral asymmetries.
<p>by Natan Horáček, Ondřej Lukšan, Zarley Rebholz, Karel Harant, Radek Pohl, Lana Mutabdžija-Nedelcheva, Simon Hellemans, Daniel Jungwirth, Jan Křivánek, Anna Amirianová, Pavlína Kyjaková, Thomas Bourguignon, Dorothea Tholl, Robert Hanus, Jitka Štáfková</p>
Termites produce the most diverse array of terpenoids among terrestrial metazoans, comprising over 200 structures. However, their biosynthesis has not yet been elucidated. Here, we identify a gene family which arose through a series of duplications of geranylgeranyl pyrophosphate synthase in the common ancestor of Neoisoptera, the terpene-producing termite lineage. We functionally characterized several proteins from this rich GGPPS-like family as terpene synthases generating biologically relevant sesqui- and diterpenes. These include the queen pheromone (3<i>R</i>,6<i>E</i>)-nerolidol in <i>Embiratermes neotenicus</i> and the presumed precursor of polycyclic defensive diterpenes (<i>E</i>,<i>E</i>,<i>E</i>)-neocembrene in <i>Nasutitermes takasagoensis</i>. We report significant enrichment of transposable elements in the GGPPS-like genomic loci, study the selection pressures acting in the evolution of the GGPPS-like family, and highlight an amino acid site crucial for cyclization capacity and enantiospecificity of the characterized enzymes. We conclude that we have identified an enzyme family that facilitated the emergence of the remarkable richness of termite terpenoids.
<p>by Cheol Soh, Mario Hervault, Nathan H. Chalkley, Kien Huynh, Qiang Zhang, Ergun Y. Uc, Jeremy D. W. Greenlee, Jan R. Wessel</p>
Response inhibition is an important cognitive control mechanism that enables flexible behavior by stopping inappropriate actions. Intracranial recordings across species have identified a neural circuit that implements response inhibition via the subthalamic nucleus of the basal ganglia. However, this work has been limited to simple tasks, in which unequivocal, salient “stop”-signals require the inhibition of all ongoing responses. Notably, response inhibition in the real world is substantially different. Real-world response inhibition is selective: it occurs only after specific salient signals (‘stimulus-selectivity’) and stops only specific movements while others continue (‘response-selectivity’). If and how the fronto-subthalamic system implements selective inhibition is largely unknown. Here, we recorded subthalamic local field potentials and scalp-EEG in humans performing a novel, selective inhibition task. Salient signals either required stopping all initiated responses (global inhibition), stopping only some responses (response-selective inhibition), or continuing all responses—i.e., ignoring the signal (which ensures stimulus-selectivity). All three signals initially triggered a common fronto-subthalamic inhibitory process, signified by a rapid increase in β-burst activity. During global inhibition, subthalamic β-bursting subsequently increased above baseline, persisting for over a second. During response-selective inhibition, this activity was delayed, which enabled a second bout of disinhibition and allowed appropriate responses to continue. Throughout this period, frontal cortical and subthalamic β-band activity were tightly coupled. This shows that selective inhibition is accompanied by rapid, context-dependent engagement and release of fronto-subthalamic inhibition. Moreover, subthalamic activity lasted substantially lon…
<p>by Jillian P. Lewis, Spencer V. Nyholm</p>
Eggs released in the environment are at risk from many threats. A recent study in PLOS Biology reveals that plastid-derived carotenoid crystals in sea urchin eggs benefit larval survival and trans-oceanic dispersal.
Eggs released in the environment are at risk from many threats. This Primer discusses how plastid-like carotenoid crystals benefit larval survival and trans-oceanic dispersal in sea urchin eggs.
<p>by Giorgia Greter, Sebastian Hummel, Daria Künzli, Naomi Dünki, Niina Ruoho, Patricia Burkhardt, Suwannee Ganguillet, Milad Radiom, Claudia Moresi, Leanid Laganenka, Wolf-Dietrich Hardt, Steffen Geisel, Julien Bauland, Sebastian Jordi, Benjamin Misselwitz, Bahtiyar Yilmaz, Jonasz Słomka, Eleonora Secchi, Roman Stocker, Emma Slack, Markus Arnoldini</p>
Spatial structure can functionally determine ecological interactions and evolution of microbial communities. The gut microbiota is known to be spatially structured longitudinally along the gastrointestinal tract, but micro-scale structure in the gut lumen has not been extensively explored. Here, we show that bacteria cluster within species in the cecum of gnotobiotic mice. We find that clustering is not driven by active swimming, antibody-mediated aggregation, or factors exclusive to the host, but likely due to bacterial growth in the matrix of gut content. In samples from mice and humans, we show that upper large-intestinal content behaves as a nonNewtonian fluid that changes its viscoelastic properties under the force of gut contractions. We argue that microbial growth in the gel-like structure of cecum content can lead to micro-scale bacterial clustering, which is periodically disrupted by peristalsis-driven shear thinning and clearance. Our study shows mechanistically how spatial structure in the gut emerges through the interplay between microbial and host physiology and highlights the possibility of host control over gut microbiota distribution through gut contractions.
<p>by Tyler J. Carrier, Andrés Rufino-Navarro, Thorben Knoop, Urska Repnik, Andrés Mauricio Caraballo-Rodríguez, David M. Needham, Corinna Bang, Sören Franzenburg, Marc Bramkamp, Willi Rath, Arne Biastoch, José Carlos Hernández, Ute Hentschel</p>
Development in the sea has long been thought to be a nutritional gamble that disproportionately ends in starvation. Here, we support the premise that components of plastids appear to be incorporated into sea urchin eggs and that these, in turn, benefit development. We find chromoplast-derived carotenoid crystals and chromoplast-specific metabolites inside the eggs of the sea urchin <i>Arbacia lixula</i>. We find evidence of plastid DNA in the eggs of 11 other sea urchins, with diatoms being the primary source and taxonomic richness of these plastid taxa directly related to egg size. The light-dependent activity of these chromoplast components influences phytohormone and lipid metabolism as well as offspring development, morphological plasticity, and survival. Offspring that benefit from these chromoplast components are predicted to disperse further, over larger geographic areas, and use a wider range of currents, including those that cross ocean basins. Data presented here challenge the long-held belief that components of non-metazoan organelles are unable to enter the germline and be passed between generations. We hypothesize that sea urchins manipulate plastids solely for their self-interest with the result of this process being a novel and adaptive form of maternal provisioning.
<p>by Chun-Jie Liu, Chao Zhang, Wei Feng, Gaoxiang Huang, Xiaopeng Zou, Wenlu Wei, Donghui Zhang</p>
Cilia dysfunction is implicated in a range of disorders. Here, we present CiliaKB, a manually curated knowledge base that serves as a one-stop platform for researchers to rapidly access mechanistic data and mine for translational clues about cilia.
Cilia dysfunction is implicated in a range of disorders. This Community Page presents CiliaKB, a manually curated knowledge base that serves as a one-stop platform for researchers to rapidly access mechanistic data and mine for translational clues about cilia.
<p>by Zhixuan Zhao, Dong-Ping Wang, Xin Zhang, Yuan Gao, Hexin Xu, Xinyu Teng, Cheng Shen, Jirui Chen, Jinru Zhang, Chang-Run Guo, Motoyuki Hattori</p>
P2X receptors are ATP-gated cation channels, and the P2X3 subtype plays crucial roles in peripheral sensory neurons, including in chronic pain and chronic cough. Accordingly, P2X3 receptors have attracted substantial interest as a therapeutic target. Gefapixant, a negative allosteric modulator (NAM) of P2X3 receptors, has been approved in some countries for the treatment of chronic cough; however, its limited selectivity for P2X3 homomers over P2X2/P2X3 heteromers is associated with taste disturbance as a prominent adverse effect. These limitations have motivated the development of next-generation NAMs with improved subtype selectivity, but their subtype-specific allosteric inhibition mechanisms are unclear. Here, we report the cryo-EM structure of the human P2X3 receptor in complex with ATP and the P2X3-selective next-generation NAM sivopixant, an investigational drug. Sivopixant binds to an allosteric site at the portal of the central pocket in the extracellular domain, and structure-based mutational analysis by electrophysiology identifies key residues required for sivopixant-dependent inhibition of human P2X3 receptors. Structural comparisons across P2X subtypes, together with patch-clamp analyses of gain-of-function mutants that confer sensitivity to two investigational drugs, sivopixant and camlipixant, provided a broadly applicable structural framework for subtype selectivity. Furthermore, structural comparisons with apo and ATP-bound open states of P2X3 receptors, together with molecular dynamics simulations, revealed that sivopixant expands the upper-body domain to suppress the lower-body movements required for channel activation, thereby preventing channel opening even in the presence of ATP.