Department of Biological Science

: Mechanism of ribosome rescue by ArfA and RF2.; ArfA rescues ribosomes stalled on truncated mRNAs by recruiting release factor RF2, which normally binds stop codons to catalyze peptide release. We report two 3.2 Å resolution cryo-EM structures - determined from a single sample - of the 70S ribosome with ArfA•RF2 in the A site. In both states, the ArfA C-terminus occupies the mRNA tunnel downstream of the A site. One state contains a compact inactive RF2 conformation. Ordering of the ArfA N-terminus in the second state rearranges RF2 into an extended conformation that docks the catalytic GGQ motif into the peptidyl-transferase center. Our work thus reveals the structural dynamics of ribosome rescue. The structures demonstrate how ArfA 'senses' the vacant mRNA tunnel and activates RF2 to mediate peptide release without a stop codon, allowing stalled ribosomes to be recycled., Keywords: ArfA, E. coli, Biochemistry, Biophysics, Release factor 2, Ribosome rescue, Stalled ribosome, Stop-codon-independent termination, Structural biology, Grant Number: R01 GM106105, R01 GM107465, Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5378476.

: Metagenome-assembled Genome Sequences Of Five Strains From The Microtus Ochrogaster (prairie Vole) Fecal Microbiome; The prairie vole (Microtus ochrogaster) is an important model for the study of social monogamy and dual parental care of offspring. Characterization of specific host species-microbe strain interactions is critical for understanding the effects of the microbiota on mood and behavior. The five metagenome-assembled genome sequences reported here represent an important step in defining the prairie vole microbiome., The publisher's version of record is availible at https://doi.org/10.1128/MRA.01310-19

: Mitochondrial Ultrastructure and Glucose Signaling Pathways Attributed to the Kv1.3 Ion Channel; Gene-targeted deletion of the potassium channel Kv1.3 (Kv1.3(-/-)) results in "Super-smeller" mice with a sensory phenotype that includes an increased olfactory ability linked to changes in olfactory circuitry, increased abundance of olfactory cilia, and increased expression of odorant receptors and the G-protein, G(olf). Kv1.3(-/-) mice also have a metabolic phenotype including lower body weight and decreased adiposity, increased total energy expenditure (TEE), increased locomotor activity, and resistance to both diet- and genetic-induced obesity. We explored two cellular aspects to elucidate the mechanism by which loss of Kv1.3 channel in the olfactory bulb (OB) may enhance glucose utilization and metabolic rate. First, using in situ hybridization we find that Kv1.3 and the insulin-dependent glucose transporter type 4 (GLUT4) are co-localized to the mitral cell layer of the OB. Disruption of Kv1.3 conduction via construction of a pore mutation (W386F Kv1.3) was sufficient to independently translocate GLUT4 to the plasma membrane in HEK 293 cells. Because olfactory sensory perception and the maintenance of action potential (AP) firing frequency by mitral cells of the OB is highly energy demanding and Kv1.3 is also expressed in mitochondria, we next explored the structure of this organelle in mitral cells. We challenged wildtype (WT) and Kv1.3(-/-) male mice with a moderately high-fat diet (MHF, 31.8 % kcal fat) for 4 months and then examined OB ultrastructure using transmission electron microscopy. In WT mice, mitochondria were significantly enlarged following diet-induced obesity (DIO) and there were fewer mitochondria, likely due to mitophagy. Interestingly, mitochondria were significantly smaller in Kv1.3(-/-) mice compared with that of WT mice. Similar to their metabolic resistance to DIO, the Kv1.3(-/-) mice had unchanged mitochondria in terms of cross sectional area and abundance following a challenge with modified diet. We are very interested to understand how targeted disruption of the Kv1.3 channel in the OB can modify TEE. Our study demonstrates that Kv1.3 regulates mitochondrial structure and alters glucose utilization; two important metabolic changes that could drive whole system changes in metabolism initiated at the OB., Keywords: brain insulin, diet-induced obesity, gated potassium channel, glucose transporter, hexose transporter, insulin-resistance, in-vivo, k+ channels, mitochondria, mouse-brain, olfactory bulb, olfactory-bulb, permeability transition, potassium channel, tyrosine phosphorylation, Publication Note: The publisher’s version of record is available at https://doi.org/10.3389/fphys.2016.00178

: Mitochondrial Ultrastructure and Glucose Signaling Pathways Attributed to the Kv1.3 Ion Channel.; Gene-targeted deletion of the potassium channel Kv1.3 (Kv1.3(-∕-)) results in "Super-smeller" mice with a sensory phenotype that includes an increased olfactory ability linked to changes in olfactory circuitry, increased abundance of olfactory cilia, and increased expression of odorant receptors and the G-protein, Golf. Kv1.3(-∕-) mice also have a metabolic phenotype including lower body weight and decreased adiposity, increased total energy expenditure (TEE), increased locomotor activity, and resistance to both diet- and genetic-induced obesity. We explored two cellular aspects to elucidate the mechanism by which loss of Kv1.3 channel in the olfactory bulb (OB) may enhance glucose utilization and metabolic rate. First, using in situ hybridization we find that Kv1.3 and the insulin-dependent glucose transporter type 4 (GLUT4) are co-localized to the mitral cell layer of the OB. Disruption of Kv1.3 conduction via construction of a pore mutation (W386F Kv1.3) was sufficient to independently translocate GLUT4 to the plasma membrane in HEK 293 cells. Because olfactory sensory perception and the maintenance of action potential (AP) firing frequency by mitral cells of the OB is highly energy demanding and Kv1.3 is also expressed in mitochondria, we next explored the structure of this organelle in mitral cells. We challenged wildtype (WT) and Kv1.3(-∕-) male mice with a moderately high-fat diet (MHF, 31.8 % kcal fat) for 4 months and then examined OB ultrastructure using transmission electron microscopy. In WT mice, mitochondria were significantly enlarged following diet-induced obesity (DIO) and there were fewer mitochondria, likely due to mitophagy. Interestingly, mitochondria were significantly smaller in Kv1.3(-∕-) mice compared with that of WT mice. Similar to their metabolic resistance to DIO, the Kv1.3(-∕-) mice had unchanged mitochondria in terms of cross sectional area and abundance following a challenge with modified diet. We are very interested to understand how targeted disruption of the Kv1.3 channel in the OB can modify TEE. Our study demonstrates that Kv1.3 regulates mitochondrial structure and alters glucose utilization; two important metabolic changes that could drive whole system changes in metabolism initiated at the OB., Keywords: Diet-induced obesity, Glucose transporter, Mitochondria, Olfactory bulb, Potassium channel, Grant Number: R01 DC003387, R01 DC013080, T32 DC000044, Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4871887.

: Modeling Dengue Virus-Hepatic Cell Interactions Using Human Pluripotent Stem Cell-Derived Hepatocyte-like Cells.; The development of dengue antivirals and vaccine has been hampered by the incomplete understanding of molecular mechanisms of dengue virus (DENV) infection and pathology, partly due to the limited suitable cell culture or animal models that can capture the comprehensive cellular changes induced by DENV. In this study, we differentiated human pluripotent stem cells (hPSCs) into hepatocytes, one of the target cells of DENV, to investigate various aspects of DENV-hepatocyte interaction. hPSC-derived hepatocyte-like cells (HLCs) supported persistent and productive DENV infection. The activation of interferon pathways by DENV protected bystander cells from infection and protected the infected cells from massive apoptosis. Furthermore, DENV infection activated the NF-κB pathway, which led to production of proinflammatory cytokines and downregulated many liver-specific genes such as albumin and coagulation factor V. Our study demonstrates the utility of hPSC-derived hepatocytes as an in vitro model for DENV infection and reveals important aspects of DENV-host interactions., Grant Number: R21 AI119530, Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5031989.

: Molecular signatures associated with ZIKV exposure in human cortical neural progenitors; Zika virus (ZIKV) infection causes microcephaly and has been linked to other brain abnormalities. How ZIKV impairs brain development and function is unclear. Here we systematically profiled transcriptomes of human neural progenitor cells exposed to Asian ZIKV(C), African ZIKV(M), and dengue virus (DENV). In contrast to the robust global transcriptome changes induced by DENV, ZIKV has a more selective and larger impact on expression of genes involved in DNA replication and repair. While overall expression profiles are similar, ZIKV(C), but not ZIKV(M), induces upregulation of viral response genes and TP53. P53 inhibitors can block the apoptosis induced by both ZIKV(C) and ZIKV(M) in hNPCs, with higher potency against ZIKV(C)-induced apoptosis. Our analyses reveal virus- and strain-specific molecular signatures associated with ZIKV infection. These datasets will help to investigate ZIKV-host interactions and identify neurovirulence determinants of ZIKV., Keywords: apoptosis, cells, expression, gene, induced hemorrhage, inhibitor, mouse model, organoids, p53, virus capsid protein, Publication Note: The publisher’s version of record is available at http://www.dx.doi.org/10.1093/nar/gkw765

: Molecular signatures associated with ZIKV exposure in human cortical neural progenitors.; Zika virus (ZIKV) infection causes microcephaly and has been linked to other brain abnormalities. How ZIKV impairs brain development and function is unclear. Here we systematically profiled transcriptomes of human neural progenitor cells exposed to Asian ZIKV, African ZIKV, and dengue virus (DENV). In contrast to the robust global transcriptome changes induced by DENV, ZIKV has a more selective and larger impact on expression of genes involved in DNA replication and repair. While overall expression profiles are similar, ZIKV, but not ZIKV, induces upregulation of viral response genes and TP53. P53 inhibitors can block the apoptosis induced by both ZIKV and ZIKV in hNPCs, with higher potency against ZIKV-induced apoptosis. Our analyses reveal virus- and strain-specific molecular signatures associated with ZIKV infection. These datasets will help to investigate ZIKV-host interactions and identify neurovirulence determinants of ZIKV., Grant Number: R01 MH102690, R01 NS051630, T32 GM008752, T32 MH015330, Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5063002.

: Multiplexed Biomarker Panels Discriminate Zika And Dengue Virus Infection In Humans; Zika virus (ZIKV) and dengue virus (DENV) are closely related flaviviruses that cause widespread, acute febrile illnesses, notably microcephaly for fetuses of infected pregnant women. Detecting the viral cause of these illnesses is paramount to determine risks to patients, counsel pregnant women, and help fight outbreaks. A combined diagnostic algorithm for ZIKV and DENV requires Reverse transcription polymerase chain reaction (RT-PCR) and IgM antibody detection. RT-PCR differentiates between DENV and ZIKV infections during the acute phases of infection, but differentiation based on IgM antibodies is currently nearly impossible in endemic areas. We have developed a ZIKV/DENV protein array and tested it with serum samples collected from ZIKV- and DENV-infected patients and healthy subjects in Puerto Rico. Our analyses reveal a biomarker panel that are capable of discriminating ZIKV and DENV infections with high accuracy, including Capsid protein from African ZIKV strain MR766, and other 5 pair of proteins (NS1, NS2A, NS3, NS4B and NS5) from ZIKV and DENV respectively. Both sensitivity and specificity of the test for ZIKV from DENV are around 90%. We propose that the ZIKV/DENV protein array will be used in future studies to discriminate patients infected with ZIKV from DENV., Keywords: identification, disease, diagnosis, antibodies, protein microarray, Publication Note: The publisher's version of record is available at https://doi.org/10.1074/mcp.RA117.000310

: Muroid rodent phylogenetics; We combined new sequence data for more than 300 muroid rodent species with our previously published sequences for up to five nuclear and one mitochondrial genes to generate the most widely and densely sampled hypothesis of evolutionary relationships across Muroidea. An exhaustive screening procedure for publically available sequences was implemented to avoid the propagation of taxonomic errors that are common to supermatrix studies. The combined data set of carefully screened sequences derived from all available sequences on GenBank with our new data resulted in a robust maximum likelihood phylogeny for 900 of the approximately 1,620 muroids. Several regions that were equivocally resolved in previous studies are now more decisively resolved, and we estimated a chronogram using 28 fossil calibrations for the most integrated age and topological estimates to date. The results were used to update muroid classification and highlight questions needing additional data. We also compared the results of multigene supermatrix studies like this one with the principal published supertrees and concluded that the latter are unreliable for any comparative study in muroids. In addition, we explored diversification patterns as an explanation for why muroid rodents represent one of the most species-rich groups of mammals by detecting evidence for increasing net diversification rates through time across the muroid tree. We suggest the observation of increasing rates may be due to a combination of parallel increases in rate across clades and high average extinction rates. Five increased diversification-rate-shifts were inferred, suggesting that multiple, but perhaps not independent, events have led to the remarkable species diversity in the superfamily. Our results provide a phylogenetic framework for comparative studies that is not highly dependent upon the signal from any one gene., Keywords: Evolution, Rodent, Nuclear DNA, Sequencing, biogeography, Publication Note: © 2017 Steppan, Schenk. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited., Preferred Citation: Steppan SJ, Schenk JJ (2017) Muroid rodent phylogenetics: 900-species tree reveals increasing diversification rates. PLoS ONE 12(8): e0183070. https://doi.org/10.1371/journal.pone.0183070, Grant Number: NSF DEB-0841447 and DEB-0454673

: Muroid rodent phylogenetics; We combined new sequence data for more than 300 muroid rodent species with our previously published sequences for up to five nuclear and one mitochondrial genes to generate the most widely and densely sampled hypothesis of evolutionary relationships across Muroidea. An exhaustive screening procedure for publically available sequences was implemented to avoid the propagation of taxonomic errors that are common to supermatrix studies. The combined data set of carefully screened sequences derived from all available sequences on GenBank with our new data resulted in a robust maximum likelihood phylogeny for 900 of the approximately 1,620 muroids. Several regions that were equivocally resolved in previous studies are now more decisively resolved, and we estimated a chronogram using 28 fossil calibrations for the most integrated age and topological estimates to date. The results were used to update muroid classification and highlight questions needing additional data. We also compared the results of multigene supermatrix studies like this one with the principal published supertrees and concluded that the latter are unreliable for any comparative study in muroids. In addition, we explored diversification patterns as an explanation for why muroid rodents represent one of the most species-rich groups of mammals by detecting evidence for increasing net diversification rates through time across the muroid tree. We suggest the observation of increasing rates may be due to a combination of parallel increases in rate across clades and high average extinction rates. Five increased diversification-rate-shifts were inferred, suggesting that multiple, but perhaps not independent, events have led to the remarkable species diversity in the superfamily. Our results provide a phylogenetic framework for comparative studies that is not highly dependent upon the signal from any one gene., Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5559066.

: Mutation-Driven Parallel Evolution during Viral Adaptation.; Convergent evolution has been demonstrated across all levels of biological organization, from parallel nucleotide substitutions to convergent evolution of complex phenotypes, but whether instances of convergence are the result of selection repeatedly finding the same optimal solution to a recurring problem or are the product of mutational biases remains unsettled. We generated 20 replicate lineages allowed to fix a single mutation from each of four bacteriophage genotypes under identical selective regimes to test for parallel changes within and across genotypes at the levels of mutational effect distributions and gene, protein, amino acid, and nucleotide changes. All four genotypes shared a distribution of beneficial mutational effects best approximated by a distribution with a finite upper bound. Parallel adaptation was high at the protein, gene, amino acid, and nucleotide levels, both within and among phage genotypes, with the most common first-step mutation in each background fixing on an average in 7 of 20 replicates and half of the substitutions in two of the four genotypes occurring at shared sites. Remarkably, the mutation of largest beneficial effect that fixed for each genotype was never the most common, as would be expected if parallelism were driven by selection. In fact, the mutation of smallest benefit for each genotype fixed in a total of 7 of 80 lineages, equally as often as the mutation of largest benefit, leading us to conclude that adaptation was largely mutation-driven, such that mutational biases led to frequent parallel fixation of mutations of suboptimal effect., Keywords: Convergence, Distribution of beneficial fitness effects, Experimental evolution, Genetics of adaptation, Mutation-driven evolution, Parallel evolution, Grant Number: T32 GM007759, Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5850295.

: Nanoscale architecture of cadherin-based cell adhesions.; Multicellularity in animals requires dynamic maintenance of cell-cell contacts. Intercellularly ligated cadherins recruit numerous proteins to form supramolecular complexes that connect with the actin cytoskeleton and support force transmission. However, the molecular organization within such structures remains unknown. Here we mapped protein organization in cadherin-based adhesions by super-resolution microscopy, revealing a multi-compartment nanoscale architecture, with the plasma-membrane-proximal cadherin-catenin compartment segregated from the actin cytoskeletal compartment, bridged by an interface zone containing vinculin. Vinculin position is determined by α-catenin, and following activation, vinculin can extend ∼30 nm to bridge the cadherin-catenin and actin compartments, while modulating the nanoscale positions of the actin regulators zyxin and VASP. Vinculin conformational activation requires tension and tyrosine phosphorylation, regulated by Abl kinase and PTP1B phosphatase. Such modular architecture provides a structural framework for mechanical and biochemical signal integration by vinculin, which may differentially engage cadherin-catenin complexes with the actomyosin machinery to regulate cell adhesions., Grant Number: 617233, Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5421576.

: Native grouper indirectly ameliorates the negative effects of invasive lionfish; Non-trophic interactions between Indo-Pacific lionfish Pterois volitans and P. miles and Atlantic and Caribbean reef fishes are not yet well understood. To determine the effects of potential competitive and behavioral interactions between native predators and invasive lionfish, we experimentally altered the presence of lionfish and red grouper Epinephelus morio in karst solution holes in Florida Bay, USA, and then tracked subsequent changes in the juvenile reef fish and motile macroinvertebrate communities for 6 wk. Relative to solution holes where we excluded both predators, mean juvenile reef fish abundance declined 83.7% in solution holes with a lionfish but increased by 154% in solution holes with a red grouper. There was no difference in juvenile reef fish abundance in solution holes with both lionfish and red grouper compared to holes where we excluded both predators. The composition of lionfish stomach contents shifted from mostly teleost fishes when lionfish were present in solution holes alone, to mostly crustaceans when in the presence of a red grouper. Concurrently, the abundance of 2 species of cleaner shrimp (Ancylomenes pedersoni and Periclimenes yucatanicus) decreased by 14.7% when lionfish were present but increased by 56.2% at holes where lionfish were excluded. We suggest that these results are due to altered lionfish predatory behavior in the presence of red grouper and highlight the importance of maintaining intact native predator communities for ameliorating the negative effects of the lionfish invasion., Keywords: caribbean sea, Community ecology, coral-reef fishes, Ecological impacts, florida-keys, indo-pacific lionfish, Interspecific interactions, Invasive species, Lionfish, mediated indirect interactions, predator, pterois-volitans, recruitment, Red grouper, red lionfish, Reef fish, shrimp, Publication Note: The publisher’s version of record is available at http://www.dx.doi.org/10.3354/meps11808

: Neuromodulation in Chemosensory Pathways.; Interactions with the environment depend not only on sensory perception of external stimuli but also on processes of neuromodulation regulated by the internal state of an organism. These processes allow regulation of stimulus detection to match the demands of an organism influenced by its general brain state (satiety, wakefulness/sleep state, attentiveness, arousal, learning etc.). The sense of smell is initiated by sensory neurons located in the nasal cavity that recognize environmental odorants and project axons into the olfactory bulb (OB), where they form synapses with several types of neurons. Modulations of early synaptic circuits are particularly important since these can affect all subsequent processing steps. While the precise mechanisms have not been fully elucidated, work from many labs has demonstrated that the activity of neurons in the OB and cortex can be modulated by different factors inducing specific changes to olfactory information processing. The symposium "Neuromodulation in Chemosensory Pathways" at the International Symposium on Olfaction and Taste (ISOT 2016) highlighted some of the most recent advances in state-dependent network modulations of the mouse olfactory system including modulation mediated by specific neurotransmitters and neuroendocrine molecules, involving pharmacological, electrophysiological, learning, and behavioral approaches., Keywords: Hormonal status, Learning, Mouse olfactory system, Network modulations, State-dependent, Surprise and expectation, Top–down inputs, Grant Number: R01 DC013090, R01 DC014690, R01 MH101293, R03 DC013988, Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5863563.

: ORF33 and ORF38 of Kaposi's Sarcoma-Associated Herpesvirus Interact and Are Required for Optimal Production of Infectious Progeny Viruses.; We recently showed that the interaction between Kaposi's sarcoma-associated herpesvirus (KSHV) tegument proteins ORF33 and ORF45 is crucial for progeny virion production, but the exact functions of KSHV ORF33 during lytic replication were unknown (J. Gillen, W. Li, Q. Liang, D. Avey, J. Wu, F. Wu, J. Myoung, and F. Zhu, J Virol 89:4918-4931, 2015, http://dx.doi.org/10.1128/JVI.02925-14). Therefore, here we investigated the relationship between ORF33 and ORF38, whose counterparts in both alpha- and betaherpesviruses interact with each other. Using specific monoclonal antibodies, we found that both proteins are expressed during the late lytic cycle with similar kinetics and that both are present in mature virions as components of the tegument. Furthermore, we confirmed that ORF33 interacts with ORF38. Interestingly, we observed that ORF33 tightly associates with the capsid, whereas ORF38 associates with the envelope. We generated ORF33-null, ORF38-null, and double-null mutants and found that these mutants apparently have identical phenotypes: the mutations caused no apparent effect on viral gene expression but reduced the yield of progeny virion by about 10-fold. The progeny virions also lack certain virion component proteins, including ORF45. During viral lytic replication, the virions associate with cytoplasmic vesicles. We also observed that ORF38 associates with the membranes of vesicles and colocalizes with the Golgi membrane or early endosome membrane. Further analyses of ORF33/ORF38 mutants revealed the reduced production of virion-containing vesicles, suggesting that ORF33 and ORF38 are involved in the transport of newly assembled viral particles into cytoplasmic vesicles, a process important for viral maturation and egress. Herpesvirus assembly is an essential step in virus propagation that leads to the generation of progeny virions. It is a complicated process that depends on the delicate regulation of interactions among virion proteins. We previously revealed an essential role of ORF45-ORF33 binding for virus assembly. Here, we report that ORF33 and its binding partner, ORF38, are required for infectious virus production due to their important role in the tegumentation process. Moreover, we found that both ORF33 and ORF38 are involved in the transportation of virions through vesicles during maturation and egress. Our results provide new insights into the important roles of ORF33 and ORF38 during viral assembly, a process critical for virus propagation that is intimately linked to KSHV pathobiology., Grant Number: F31 CA183250, R01DE016680, R01 DE016680, HHSN261200800001E, HHSN261200800001C, HHSN261200800001E, Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4734004.

: Ocean acidification changes the male fitness landscape; Sperm competition is extremely common in many ecologically important marine taxa. Ocean acidification (OA) is driving rapid changes to the marine environments in which freely spawned sperm operate, yet the consequences of OA on sperm performance are poorly understood in the context of sperm competition. Here, we investigated the impacts of OA (+ 1000 mu atm pCO(2)) on sperm competitiveness for the sea urchin Paracentrotus lividus. Males with faster sperm had greater competitive fertilisation success in both seawater conditions. Similarly, males with more motile sperm had greater sperm competitiveness, but only under current pCO(2) levels. Under OA the strength of this association was significantly reduced and there were male sperm performance rank changes under OA, such that the best males in current conditions are not necessarily best under OA. Therefore OA will likely change the male fitness landscape, providing a mechanism by which environmental change alters the genetic landscape of marine species., Keywords: arenicola-marina, egg size, fertilization success, gamete age, motility, near-future levels, ph, sea-urchin, spawning marine invertebrate, sperm competition, Publication Note: The publisher’s version of record is available at https://doi.org/10.1038/srep31250

: Ocean acidification changes the male fitness landscape.; Sperm competition is extremely common in many ecologically important marine taxa. Ocean acidification (OA) is driving rapid changes to the marine environments in which freely spawned sperm operate, yet the consequences of OA on sperm performance are poorly understood in the context of sperm competition. Here, we investigated the impacts of OA (+1000 μatm pCO2) on sperm competitiveness for the sea urchin Paracentrotus lividus. Males with faster sperm had greater competitive fertilisation success in both seawater conditions. Similarly, males with more motile sperm had greater sperm competitiveness, but only under current pCO2 levels. Under OA the strength of this association was significantly reduced and there were male sperm performance rank changes under OA, such that the best males in current conditions are not necessarily best under OA. Therefore OA will likely change the male fitness landscape, providing a mechanism by which environmental change alters the genetic landscape of marine species., Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4987666.

: Open chromatin reveals the functional maize genome.; Cellular processes mediated through nuclear DNA must contend with chromatin. Chromatin structural assays can efficiently integrate information across diverse regulatory elements, revealing the functional noncoding genome. In this study, we use a differential nuclease sensitivity assay based on micrococcal nuclease (MNase) digestion to discover open chromatin regions in the maize genome. We find that maize MNase-hypersensitive (MNase HS) regions localize around active genes and within recombination hotspots, focusing biased gene conversion at their flanks. Although MNase HS regions map to less than 1% of the genome, they consistently explain a remarkably large amount (∼40%) of heritable phenotypic variance in diverse complex traits. MNase HS regions are therefore on par with coding sequences as annotations that demarcate the functional parts of the maize genome. These results imply that less than 3% of the maize genome (coding and MNase HS regions) may give rise to the overwhelming majority of phenotypic variation, greatly narrowing the scope of the functional genome., Keywords: Biased gene conversion, Chromatin, Maize, Recombination, Variance partitioning, Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896728.

: Pathways For Effects Of Small-scale Disturbances On A Rare Plant; Small-scale soil disturbances such as soil mounds produced by gophers are known to influence local plant communities. A variety of mechanisms might account for the influence of gopher disturbances on individual plant success, but understanding of these mechanisms is not well developed. Disturbances are often assumed to affect plants through changing competition or the abiotic environment, but disturbances might also influence plant size, which in turn influences other biotic interactions, including pollination. In this study, we tested for effects of soil disturbance on the density, flower size, and reproduction of an annual plant, Mimulus angustatus. We used soil disturbance manipulations, observational data, and a pollination experiment to examine two possible pathways for effects of disturbance on M. angustatus: competition and pollination. We also considered how effects of gopher mounds change with years since initial disturbance. We found that disturbance strongly increased the local density and flower size of M. angustatus, but the strength of these effects decays quickly. We found no support for these effects being mediated by competition with other plant species. We also found that M. angustatus with larger flowers receive more natural pollination. Our pollination experiment suggests that M. angustatus benefits from pollination (seed set increases with hand pollination or access to pollinators), and suggests that pollen limitation may occur. Taken together, our results indicate that increased pollination and seed set is an alternative response to disturbance that should receive further consideration. Regardless of the exact mechanism, it appears that in the absence of frequent small-scale soil disturbance, M. angustatus would not persist at our field site, as a large majority of plant recruitment and seed set occurs on recent disturbances., Keywords: disturbance, diversity, dynamics, establishment, grassland, heterogeneity, local density, mating system, mechanisms, patterns, penstemon-grandiflorus, plant size, pocket gophers, pollen limitation, pollination, reproduction, Publication Note: The publisher's version of record is available at https://doi.org/10.1002/ecs2.1838

: Pearson 2018 Associated taxon records parsing R code; Publication Note: The published research is funded by the National Science Foundation. This R code is under an Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) license., Grant Number: 1547229

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