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UFGI publication round-up week 3/5

J Am Heart Assoc. 2018 Mar 9;7(6). pii: e007339. doi: 10.1161/JAHA.117.007339.

Genome Wide Association Study Identifies the HMGCS2 Locus to be Associated With Chlorthalidone Induced Glucose Increase in Hypertensive Patients.

Author information

1
Department of Pharmacotherapy and Translational Research and Center for Pharmacogenomics, University of Florida, Gainesville, FL.
2
Department of Pathology, Center of Regenerative Medicine, University of Florida, Gainesville, FL.
3
Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN.
4
Department of Medicine, University of Maryland, Baltimore, MD.
5
Human Genetics and Institute of Molecular Medicine, University of Texas Health Science Center, Houston, TX.
6
Section of Nephrology, University of Chicago, IL.
7
Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN.
8
Department of Pharmacotherapy and Translational Research and Center for Pharmacogenomics, University of Florida, Gainesville, FL dehoff@cop.ufl.edu.
9
Division of Cardiovascular Medicine, Department of Medicine, University of Florida, Gainesville, FL.

Abstract

BACKGROUND:

Thiazide and thiazide-like diuretics are first-line medications for treating uncomplicated hypertension. However, their use has been associated with adverse metabolic events, including hyperglycemia and incident diabetes mellitus, with incompletely understood mechanisms. Our goal was to identify genomic variants associated with thiazide-like diuretic/chlorthalidone-induced glucose change.

METHODS AND RESULTS:

Genome-wide analysis of glucose change after treatment with chlorthalidone was performed by race among the white (n=175) and black (n=135) participants from the PEAR-2 (Pharmacogenomic Evaluation of Antihypertensive Responses-2). Single-nucleotide polymorphisms with P<5×10-8 were further prioritized using in silico analysis based on their expression quantitative trait loci function. Among blacks, an intronic single-nucleotide polymorphism (rs9943291) in the HMGCS2 was associated with increase in glucose levels following chlorthalidone treatment (ß=12.5; P=4.17×10-8). G-allele carriers of HMGCS2 had higher glucose levels (glucose change=+16.29 mg/dL) post chlorthalidone treatment compared with noncarriers of G allele (glucose change=+2.80 mg/dL). This association was successfully replicated in an independent replication cohort of hydrochlorothiazide-treated participants from the PEAR study (ß=5.54; P=0.023). A meta-analysis of the 2 studies was performed by race in Meta-Analysis Helper, where this single-nucleotide polymorphism, rs9943291, was genome-wide significant with a meta-analysis P value of 3.71×10-8HMGCS2, a part of the HMG-CoA synthase family, is important for ketogenesis and cholesterol synthesis pathways that are essential in glucose homeostasis.

CONCLUSIONS:

These results suggest that HMGCS2 is a promising candidate gene involved in chlorthalidone and Hydrochlorothiazide (HCTZ)-induced glucose change. This may provide insights into the mechanisms involved in thiazide-induced hyperglycemia that may ultimately facilitate personalized approaches to antihypertensive selection for hypertension treatment.

 
 

J Pharm Sci. 2018 Mar 5. pii: S0022-3549(18)30138-2. doi: 10.1016/j.xphs.2018.02.021. [Epub ahead of print]

Quantitative estimation of plasma free drug fraction in patients with varying degrees of hepatic impairment: a methodological evaluation.

Author information

1
Center for Drug Clinical Research, Shanghai University of Chinese Medicine, Shanghai 201203, China; Department of Pharmaceutics, College of Pharmacy, University of Florida, Gainesville, FL 32610, USA.
2
Subei People’s Hospital, Yangzhou University, Yangzhou, Jiangsu 225001, China; Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
3
Center for Drug Clinical Research, Shanghai University of Chinese Medicine, Shanghai 201203, China.
4
School of Pharmaceutical Sciences, Shandong University, Jinan, Shandong 250012, China.
5
Center for Drug Clinical Research, Shanghai University of Chinese Medicine, Shanghai 201203, China. Electronic address: qingshan.q.zheng@gmail.com.
6
Department of Pharmaceutics, College of Pharmacy, University of Florida, Gainesville, FL 32610, USA. Electronic address: qingshan.q.zheng@gmail.com.

Abstract

Quantitative prediction of unbound drug fraction (fu) is essential for scaling pharmacokinetics through physiologically-based approaches. However, few attempts have been made to evaluate the projection of fu values under pathological conditions. The primary objective of this study was to predict fu values (n=105) of 56 compounds with or without the information of predominant binding protein in patients with varying degrees of hepatic insufficiency by accounting for quantitative changes in molar concentrations of either the major binding protein or albumin plus alpha 1-acid glycoprotein (AAG) associated with differing levels of hepatic dysfunction. For the purpose of scaling, data pertaining to albumin and AAG levels in response to differing degrees of hepatic impairment were systematically collected from 946 adult donors. The results of the present study demonstrate for the first time the feasibility of physiologically-based scaling fu in hepatic dysfunction after verifying with experimentally measured data of a wide variety of compounds from individuals with varying degrees of hepatic insufficiency. Furthermore, the high level of predictive accuracy indicates that the interrelation between the severity of hepatic impairment and these plasma protein levels are physiologically accurate. The current work enhances the confidence in predicting fu in hepatic insufficiency, particularly for albumin-bound drugs.

 
 

Microbiology. 2018 Mar 8. doi: 10.1099/mic.0.000644. [Epub ahead of print]

Hydrophobins contribute to root colonization and stress responses in the rhizosphere-competent insect pathogenic fungus Beauveria bassiana.

Author information

1
1​Department of Biological Sciences, Brock University, St. Catharines, ON L2S 3A1, Canada.
2
2​Department of Microbiology and Cell Science, University of Florida, Gainesville, FL 32611, USA.

Abstract

The hyd1/hyd2 hydrophobins are important constituents of the conidial cell wall of the insect pathogenic fungus Beauveria bassiana. This fungus can also form intimate associations with several plant species. Here, we show that inactivation of two Class I hydrophobin genes, hyd1 or hyd2, significantly decreases the interaction of B. bassiana with bean roots. Curiously, the ∆hyd1/∆hyd2 double mutant was less impaired in root association than Δhyd1 or Δhyd2. Loss of hyd genes affected growth rate, conidiation ability and oosporein production. Expression patterns for genes involved in conidiation, cell wall integrity, insect virulence, signal transduction, adhesion, hydrophobicity and oosporein production were screened in the deletion mutants grown in different conditions. Repression of the major MAP-Kinase signal transduction pathways (Slt2 MAPK pathway) was observed that was more pronounced in the single versus double hyd mutants under certain conditions. The ∆hyd1/∆hyd2 double mutant showed up-regulation of the Hog1 MAPK and the Msn2 transcription factor under certain conditions when compared to the wild-type or single hyd mutants. The expression of the bad2 adhesin and the oosporein polyketide synthase 9 gene was severely reduced in all of the mutants. On the other hand, fewer changes were observed in the expression of key conidiation and cell wall integrity genes in hyd mutants compared to wild-type. Taken together, the data from this study indicated pleiotropic consequences of deletion of hyd1 and hyd2 on signalling and stress pathways as well as the ability of the fungus to form stable associations with plant roots.

 
 

J Virol. 2018 Mar 7. pii: JVI.00173-18. doi: 10.1128/JVI.00173-18. [Epub ahead of print]

Depletion of the insulator protein CTCF results in HSV-1 reactivation in vivo.

Author information

1
Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, LA.
2
Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, FL.
3
Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, LA dneum1@lsuhsc.edu.
4
Department of Ophthalmology, LSU Eye Center of Excellence, New Orleans, LA.

Abstract

Herpes Simplex Virus 1 (HSV-1) establishes a lifelong latent infection in host peripheral neurons including the neurons of the trigeminal ganglia (TG). HSV-1 can reactivate from neurons to cause recurrent infection. During latency, the insulator protein CTCF occupies DNA binding sites on the HSV-1 genome and these sites have been previously characterized as functional enhancer-blocking insulators. Previously, CTCF was found to be dissociated from wild type virus post-reactivation but not in mutants that do not reactivate, indicating that CTCF eviction may also be an important component of reactivation. To further elucidate the role of CTCF in reactivation of HSV-1, we used recombinant adeno-associated virus (rAAV) vectors to deliver an siRNA targeting CTCF to peripheral neurons latent with HSV-1 in rabbit TG. Our data show that CTCF depletion resulted in long-term and persistent shedding of infectious virus in the cornea and increased ICP0 expression in the ganglia, indicating that CTCF depletion facilitates HSV-1 reactivation.IMPORTANCE Increasing evidence has shown that the insulator protein CTCF regulates gene expression of DNA viruses, including the gammaherpesviruses. While CTCF occupation and insulator function control gene expression in DNA viruses, CTCF eviction has been correlated to increased lytic gene expression and the dissolution of transcriptional domains. Our previous data have shown that in the alphaherpesvirus HSV-1, CTCF was found to be dissociated from the HSV-1 genome post-reactivation, further indicating a global role for CTCF eviction in the transition from latency to reactivation in HSV-1 genomes. Using an rAAV8, we targeted HSV-1 infected peripheral neurons for CTCF depletion to show that CTCF depletion precedes the shedding of infectious virus and increased lytic gene expression in vivo, providing the first evidence that CTCF depletion facilitates HSV-1 reactivation.

 
 

Cell Rep. 2018 Mar 6;22(10):2667-2676. doi: 10.1016/j.celrep.2018.02.032.

α Cell Function and Gene Expression Are Compromised in Type 1 Diabetes.

Author information

1
Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, Vanderbilt University Medical Center, Nashville, TN, USA. Electronic address: marcela.brissova@vanderbilt.edu.
2
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, USA.
3
HudsonAlpha Institute for Biotechnology, Huntsville, AL, USA.
4
Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, Vanderbilt University Medical Center, Nashville, TN, USA.
5
Department of Medicine, Diabetes Division, Diabetes Center of Excellence, University of Massachusetts Medical School, Worcester, MA, USA; Math and Science Division, Babson College, Wellesley, MA 02457, USA.
6
Institute of Cellular Therapeutics, Allegheny-Singer Research Institute, Allegheny Health Network, Pittsburgh, PA, USA.
7
Department of Pathology, University of Florida Diabetes Institute, College of Medicine, Gainesville, FL, USA.
8
Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA.
9
Type 1 Diabetes Center, the La Jolla Institute for Allergy and Immunology, La Jolla, CA, USA.
10
Department of Medicine, Diabetes Division, Diabetes Center of Excellence, University of Massachusetts Medical School, Worcester, MA, USA.
11
The Jackson Laboratory, Bar Harbor, ME, USA.
12
Departments of Medicine and Pediatrics, Section of Endocrinology, Diabetes, and Metabolism, University of Chicago, Chicago, IL, USA.
13
Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA.
14
Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, USA; Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN, USA. Electronic address: al.powers@vanderbilt.edu.

Abstract

Many patients with type 1 diabetes (T1D) have residual β cells producing small amounts of C-peptide long after disease onset but develop an inadequate glucagon response to hypoglycemia following T1D diagnosis. The features of these residual β cells and α cells in the islet endocrine compartment are largely unknown, due to the difficulty of comprehensive investigation. By studying the T1D pancreas and isolated islets, we show that remnant β cells appeared to maintain several aspects of regulated insulin secretion. However, the function of T1D α cells was markedly reduced, and these cells had alterations in transcription factors constituting α and β cell identity. In the native pancreas and after placing the T1D islets into a non-autoimmune, normoglycemic in vivo environment, there was no evidence of α-to-β cell conversion. These results suggest an explanation for the disordered T1D counterregulatory glucagon response to hypoglycemia.

 
 

J Clin Pharmacol. 2018 Mar 7. doi: 10.1002/jcph.1088. [Epub ahead of print]

Core Entrustable Professional Activities in Clinical Pharmacology: Pearls for Clinical Practice: Drug-Drug and Food-Drug Interactions.

Author information

1
Clinical Research Appliance, Gelnhausen, Germany.
2
Faculty of the International Marbach DDI Workshop Organisation.
3
Department of Pharmaceutics, College of Pharmacy, University of Florida, Gainesville, FL, USA.
4
Clinical Pharmacology, Sandoz Biopharmaceuticals, Holzkirchen, Germany.
5
Centre for Applied Pharmacokinetic Research (CAPKR), University of Manchester, UK.

 
 

Sci Rep. 2018 Mar 6;8(1):4049. doi: 10.1038/s41598-018-21371-4.

Characterization of gene regulation and protein interaction networks for Matrin 3 encoding mutations linked to amyotrophic lateral sclerosis and myopathy.

Author information

1
Department of Neuroscience, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, University of Florida, Gainesville, FL, USA.
2
Department of Molecular Genetics & Microbiology, Center for Neurogenetics, Genetics Institute, University of Florida, Gainesville, FL, USA.
3
Department of Pharmacology & Therapeutics, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, University of Florida, Gainesville, FL, USA.
4
Department of Neuroscience, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, University of Florida, Gainesville, FL, USA. drb1@ufl.edu.

Abstract

To understand how mutations in Matrin 3 (MATR3) cause amyotrophic lateral sclerosis (ALS) and distal myopathy, we used transcriptome and interactome analysis, coupled with microscopy. Over-expression of wild-type (WT) or F115C mutant MATR3 had little impact on gene expression in neuroglia cells. Only 23 genes, expressed at levels of >100 transcripts showed ≥1.6-fold changes in expression by transfection with WT or mutant MATR3:YFP vectors. We identified ~123 proteins that bound MATR3, with proteins associated with stress granules and RNA processing/splicing being prominent. The interactome of myopathic S85C and ALS-variant F115C MATR3 were virtually identical to WT protein. Deletion of RNA recognition motif (RRM1) or Zn finger motifs (ZnF1 or ZnF2) diminished the binding of a subset of MATR3 interacting proteins. Remarkably, deletion of the RRM2 motif caused enhanced binding of >100 hundred proteins. In live cells, MATR3 lacking RRM2 (ΔRRM2) formed intranuclear spherical structures that fused over time into large structures. Our findings in the cell models used here suggest that MATR3 with disease-causing mutations is not dramatically different from WT protein in modulating gene regulation or in binding to normal interacting partners. The intra-nuclear localization and interaction network of MATR3 is strongly modulated by its RRM2 domain.

 
 

Neonatology. 2018 Mar 6;113(4):347-352. doi: 10.1159/000487848. [Epub ahead of print]

Enteral Feeding as an Adjunct to Hypothermia in Neonates with Hypoxic-Ischemic Encephalopathy.

Author information

1
Department of Pediatrics, University of Florida, Gainesville, Florida, USA.
2
UF Health Jacksonville, Jacksonville, Florida, USA.
3
St. Joseph’s Hospital Tampa, Tampa, Florida, USA.
4
Department of Radiology, University of Florida, Gainesville, Florida, USA.
5
Department of Agricultural and Biological Engineering, Biostatistics and Statistics, University of Florida, Gainesville, Florida, USA.

Abstract

BACKGROUND:

Withholding enteral feedings during hypothermia lacks supporting evidence.

OBJECTIVES:

We aimed to determine if minimal enteral nutrition (MEN) during hypothermia in patients with hypoxic-ischemic encephalopathy was associated with a reduced duration of parenteral nutrition, time to full oral feeds, and length of stay, but would not be associated with increased systemic inflammation or feeding complications.

METHODS:

We performed a pilot, retrospective, matched case-control study within the Florida Neonatal Neurologic Network from December 2012 to May 2016 of patients who received MEN during hypothermia (n = 17) versus those who were not fed (n = 17). Length of stay, feeding-related outcomes, and brain injury identified by MRI were compared. Serum inflammatory mediators were measured at 0-6, 24, and 96 h of life by multiplex assay. MRI were scored using the Barkovich system.

RESULTS:

MEN subjects had a reduced length of hospital stay (mean 15 ± 11 vs. 24 ± 19 days, p < 0.05), days receiving parenteral nutrition (7 ± 2 vs. 11 ± 6, p < 0.05), and time to full oral feeds (8 ± 5 vs. 18 ± 18, p < 0.05). MEN was associated with a significantly reduced serum IL-12p70 at 24 and 96 h (p < 0.05). Brain MRI scores were not significantly different between groups.

CONCLUSION:

MEN during hypothermia was associated with a reduced length of stay and time to full feeds, but did not increase feeding complications or systemic inflammation.

 
 

Ecol Appl. 2018 Mar 6. doi: 10.1002/eap.1682. [Epub ahead of print]

Satellite sensor requirements for monitoring essential biodiversity variables of coastal ecosystems.

Author information

1
College of Marine Science, University of South Florida, 140 7th Avenue South, Saint Petersburg, Florida, 33701, USA.
2
School of Engineering, University of California Merced, 5200 N. Lake Road, Merced, California, 95340, USA.
3
Joint Center for Earth Systems Technology, University of Maryland, 5523 Research Park Drive, Baltimore, Maryland, 21228, USA.
4
Department of Geography, University of Southern California, Santa Barbara, California, 93106, USA.
5
Applied Physics Lab, Johns Hopkins University, 11100 Johns Hopkins Road, Laurel, Maryland, 20723, USA.
6
Scripps Institution of Oceanography, University of California San Diego, La Jolla, California, 92093, USA.
7
Commonwealth Scientific and Industrial Research Organisation, Canberra, Australian Capital Territory, Australia.
8
Stetson University College of Law, 1401 61st Street South, Gulfport, Florida, 33707, USA.
9
HySpeed Computing, Miami, Florida, 33143, USA.
10
U.S. Environmental Protection Agency, National Exposure Research Laboratory, Research Triangle Park, Raleigh, North Carolina, 27711, USA.
11
Ocean Ecology Laboratory, Goddard Space Flight Center, National Aeronautics and Space Administration, Greenbelt, Maryland, 20770, USA.
12
Goddard Space Flight Center, Science Systems and Applications, Greenbelt, Maryland, 20770, USA.
13
Naval Research Laboratory, Washington, D.C., 20375, USA.
14
Department of Geography, University of California Los Angeles, Los Angeles, California, 90095, USA.
15
Goddard Institute for Space Studies, Columbia University, New York, New York, 10025, USA.
16
City University of New York, New York, New York, 10031, USA.
17
School of Marine Sciences, University of Maine, Orono, Maine, 04469, USA.
18
Jet Propulsion Laboratory, California Institute of Technology, Pasadena, California, 91109, USA.
19
Universities Space Research Association, Goddard Space Flight Center, National Aeronautics and Space Administration, Greenbelt, Maryland, 20770, USA.
20
NOAA Geophysical Fluid Dynamics Laboratory, Princeton, New Jersey, 08540, USA.
21
Climate and Global Dynamics Laboratory, University Corporation for Atmospheric Research, Boulder, Colorado, 80301, USA.
22
Laboratorio de Sensores Remotos, Universidad Simon Bolívar, Sartenejas, Apartado, Caracas, 89000, Venezuela.
23
Lamont Doherty Earth Observatory, Columbia University, Palisades, New York, 10964, USA.
24
College of Oceanic and Atmospheric Science, Oregon State University, Corvallis, Oregon, 97331, USA.
25
Roffer’s Ocean Fishing Forecasting Service, 60 Westover Drive, West Melbourne, Florida, 32904, USA.
26
Alfred Wegener Institute Helmholtz Centre for Polar and Marine Research, Bremerhaven, Germany.
27
Stanford University, Stanford, California, 94305, USA.
28
Department of Marine Sciences, University of Connecticut, Groton, Connecticut, 06340, USA.
29
Earth System Science and Policy, University of North Dakota, Grand Forks, North Dakota, 58202, USA.
30
Bren School of Environmental Science and Management, University of California, Santa Barbara, California, 93106, USA.
31
EcoQuants, 508 East Haley Street, Santa Barbara, California, 93103, USA.
32
Florida Museum of Natural History, University of Florida, Cultural Plaza, 3215 Hull Road, Gainesville, Florida, 32611, USA.
33
Wallops Flight Facility, NASA Goddard Space Flight Center, Wallops Island, Virginia, 23337, USA.
34
Woods Hole Oceanographic Institution, Woods Hole, Massachusetts, 02543, USA.
35
University of California Santa Cruz, Santa Cruz, California, 95064, USA.
36
Graduate School of Oceanography, University of Rhode Island, Kingston, Rhode Island, 02881, USA.
37
WET Labs/Sea-Bird Scientific, P.O. Box 518, Philomath, Oregon, 97370, USA.
38
Airborne Science Program, NASA Ames Research Center, Moffett Field, California, 94035, USA.
39
Department of Earth and Oceanographic Science, Bowdoin College, Brunswick, Maine, 04011, USA.
40
Geo-Information Science and Earth Observation (ITC), University of Twente, Enschede, The Netherlands.
41
Intergovernmental Oceanographic Commission of UNESCO, Ocean Biogeographic Information System, Oostende, Belgium.
42
Department of Ecology and Evolutionary Biology, Yale University, New Haven, Connecticut, 06511, USA.

Abstract

The biodiversity and high productivity of coastal terrestrial and aquatic habitats are the foundation for important benefits to human societies around the world. These globally distributed habitats need frequent and broad systematic assessments, but field surveys only cover a small fraction of these areas. Satellite-based sensors can repeatedly record the visible and near-infrared reflectance spectra that contain the absorption, scattering, and fluorescence signatures of functional phytoplankton groups, colored dissolved matter, and particulate matter near the surface ocean, and of biologically structured habitats (floating and emergent vegetation, benthic habitats like coral, seagrass, and algae). These measures can be incorporated into Essential Biodiversity Variables (EBVs), including the distribution, abundance, and traits of groups of species populations, and used to evaluate habitat fragmentation. However, current and planned satellites are not designed to observe the EBVs that change rapidly with extreme tides, salinity, temperatures, storms, pollution, or physical habitat destruction over scales relevant to human activity. Making these observations requires a new generation of satellite sensors able to sample with these combined characteristics: (1) spatial resolution on the order of 30 to 100-m pixels or smaller; (2) spectral resolution on the order of 5 nm in the visible and 10 nm in the short-wave infrared spectrum (or at least two or more bands at 1,030, 1,240, 1,630, 2,125, and/or 2,260 nm) for atmospheric correction and aquatic and vegetation assessments; (3) radiometric quality with signal to noise ratios (SNR) above 800 (relative to signal levels typical of the open ocean), 14-bit digitization, absolute radiometric calibration <2%, relative calibration of 0.2%, polarization sensitivity <1%, high radiometric stability and linearity, and operations designed to minimize sunglint; and (4) temporal resolution of hours to days. We refer to these combined specifications as H4 imaging. Enabling H4 imaging is vital for the conservation and management of global biodiversity and ecosystem services, including food provisioning and water security. An agile satellite in a 3-d repeat low-Earth orbit could sample 30-km swath images of several hundred coastal habitats daily. Nine H4 satellites would provide weekly coverage of global coastal zones. Such satellite constellations are now feasible and are used in various applications.

 
 

Mol Ther. 2018 Mar 7;26(3):669-671. doi: 10.1016/j.ymthe.2018.02.009. Epub 2018 Mar 1.

Safety First: Perspective on Patient-Centered Development of AAV Gene Therapy Products.

Author information

1
Department of Pediatrics and Molecular Genetics & Microbiology, College of Medicine, University of Florida, Gainesville 32611, FL, USA. Electronic address: bbyrne@ufl.edu.

 
 

Curr Biol. 2018 Mar 5;28(5):770-778.e5. doi: 10.1016/j.cub.2018.01.061. Epub 2018 Feb 15.

A Comprehensive and Dated Phylogenomic Analysis of Butterflies.

Author information

1
Arthropoda Department, Zoological Research Museum Alexander Koenig, Adenauer Allee 160, 53113 Bonn, Germany; Florida Museum of Natural History, University of Florida, Gainesville, FL 32611, USA; Museum of Comparative Zoology, Harvard University, Cambridge, MA 02138, USA. Electronic address: m.espeland@leibniz-zfmk.de.
2
Florida Museum of Natural History, University of Florida, Gainesville, FL 32611, USA; RAPiD Genomics 747 SW 2nd Avenue IMB#14, Gainesville, FL 32601, USA.
3
Florida Museum of Natural History, University of Florida, Gainesville, FL 32611, USA.
4
Institut de Biologia Evolutiva (CSIC- Universitat Pompeu Fabra), Passeig Marítim de la Barceloneta 37, ESP-08003 Barcelona, Spain.
5
Museum of Comparative Zoology, Harvard University, Cambridge, MA 02138, USA.
6
Biology Department, City College of New York, New York, NY 10031, USA.
7
Museum of Comparative Zoology, Harvard University, Cambridge, MA 02138, USA; Institut de Biologia Evolutiva (CSIC- Universitat Pompeu Fabra), Passeig Marítim de la Barceloneta 37, ESP-08003 Barcelona, Spain.
8
Institute for Agricultural Sciences, Biocommunication & Entomology, Eidgenössische Technische Hochschule Zürich (ETHZ), WEV E26.1, Weinbergstrasse 56-58, 8092 Zürich, Switzerland.
9
Department of Ecology and Evolutionary Biology, Yale University, New Haven, CT 06511-8934, USA.
10
Biology Department, City College of New York, New York, NY 10031, USA; PhD Program in Biology, Graduate Center, City University of New York, New York, NY 10016, USA; Entomology Section, National Museum of the Philippines, Manila 1000, Philippines.
11
Florida Museum of Natural History, University of Florida, Gainesville, FL 32611, USA. Electronic address: kawahara@flmnh.ufl.edu.

Abstract

Butterflies (Papilionoidea), with over 18,000 described species [1], have captivated naturalists and scientists for centuries. They play a central role in the study of speciation, community ecology, biogeography, climate change, and plant-insect interactions and include many model organisms and pest species [2, 3]. However, a robust higher-level phylogenetic framework is lacking. To fill this gap, we inferred a dated phylogeny by analyzing the first phylogenomic dataset, including 352 loci (> 150,000 bp) from 207 species representing 98% of tribes, a 35-fold increase in gene sampling and 3-fold increase in taxon sampling over previous studies [4]. Most data were generated with a new anchored hybrid enrichment (AHE) [5] gene kit (BUTTERFLY1.0) that includes both new and frequently used (e.g., [6]) informative loci, enabling direct comparison and future dataset merging with previous studies. Butterflies originated around 119 million years ago (mya) in the late Cretaceous, but most extant lineages diverged after the Cretaceous-Paleogene (K-Pg) mass-extinction 65 mya. Our analyses support swallowtails (Papilionidae) as sister to all other butterflies, followed by skippers (Hesperiidae) + the nocturnal butterflies (Hedylidae) as sister to the remainder, indicating a secondary reversal from diurnality to nocturnality. The whites (Pieridae) were strongly supported as sister to brush-footed butterflies (Nymphalidae) and blues + metalmarks (Lycaenidae and Riodinidae). Ant association independently evolved once in Lycaenidae and twice in Riodinidae. This study overturns prior notions of the taxon’s evolutionary history, as many long-recognized subfamilies and tribes are para- or polyphyletic. It also provides a much-needed backbone for a revised classification of butterflies and for future comparative studies including genome evolution and ecology.

 
 

NOTE: These abstracts were retrieved from the U.S. National Library of Medicine website managed in collaboration with the U.S. National Library of Medicine

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