FULL POSTER SESSION ABSTRACTSbinding module, are also increased relative to brown-rot fungi. Indeed, secretomic analysis identified GH6, GH7, CDH and PMO peptides only in white-rotfungi. Overall, these results show that, relative to brown rot fungi, white rot polyporales maintain greater enzymatic diversity supporting lignocelluloseattack.248. Genomic context and distribution of effector genes in Fusarium oxysporum. Sarah Maria Schmidt 1 , Peter van Dam 1 , Petra M. Houterman 1 , InesSchreiver 2 , Lisong Ma 1 , Stephan Amyotte 3 , Biju Chellappan 1 , Sjef Boeren 4 , Frank L.W. Takken 1 , Martijn Rep 1 . 1) Molecular Plant Pathology, SwammerdamInstitute for Life Sciences, University of Amsterdam, Science Park 904, 1098 XH Amsterdam, the Netherlands; 2) Fachgebiet Medizinische Biotechnologie,Institut für Biotechnologie, Technische Universität Berlin, Gustav-Meyer-Allee 25, Germany; 3) Department of Plant Pathology, University of Kentucky,201F Plant Science Building, 1405 Veterans Drive, Lexington, KY 40546-0312, USA; 4) Laboratory for Biochemistry, Wageningen University, Dreijenlaan 3,6703HA, Wageningen, the Netherlands.Strains of the Fusarium oxysporum species complex (FOSC) are able to infect a wide range of mono- and dicotyledonous plants. Based on the hostspecificity of individual strains, the FOSC is divided into various formae speciales. All strains share a common core genome and possess additional lineagespecific(LS) chromosomes. The fungus secretes effector proteins into the host vascular system that presumably manipulate the host to promote infection.In the tomato pathogen F. oxysporum f. sp. lycopersici (Fol) these effectors are encoded by SIX (Secreted In Xylem) genes. Interestingly, all SIX genes arepresent on a single LS chromosome that can be transferred horizontally to a previously non-pathogenic Fo strain, resulting in gain of pathogenicity towardstomato. Upon close inspection of this tomato pathogenicity chromosome we discovered that a non-autonomous miniature transposable element (mite) ispresent in the promoters of all SIX genes. Promoter deletion analysis at two different SIX gene loci did not reveal a direct role of the mite for SIX geneexpression. However, we were able to use this genomic signature to predict novel effector gene candidates in the Fol genome. Expression of several ofthese novel candidates during infection was confirmed by mass spectroscopic analysis of the xylem sap of Fol-infected tomato plants. We also discovered asmall reservoir of ‘silent’ effector genes that are not expressed during infection. Next, we used our method to predict effector gene candidates in thegenomes of several other formae speciales and developed a more global picture of the effector gene complement in the FOSC. Effector genes in Foconsistently reside in repeat-rich enviroments. Some strains contain 2 or 3 paralogs of an effector gene. Additionally, many genomes feature truncatedeffector gene homologs. Overall, the effector gene distribution among different formae speciales is patchy, and there is no unique set of effectors that iscommon to all plant pathogenic strains of the FOSC.249. Whole genome sequencing reveals new links between diverse plant pathogens; an expanded AvrLm6-like gene family in Venturia species. JasonShiller 1 , Angela van de Wouw 2 , Dan Jones 1 , Joanna Bowen 3 , Carl Mesarich 3 , Matthew Templeton 3 , Kim Plummer 1 . 1) La Trobe University, Melbourne,Australia; 2) University of Melbourne, Melbourne, Australia; 3) Plant and Food Research, Auckland, New Zealand.Venturia inaequalis and V. pirina are hemi-biotrophic fungi that cause apple scab and pear scab, respectively. These diseases cause significant losses togrowers worldwide. In some cases, scab is controlled with resistant cultivars, but fungicides are more commonly used. Resistance to scab follows the genefor-genemodel, whereby a gene coding for a resistance protein in the host will have a cognate gene coding for an avirulence protein (or effector) in thefungus. No Venturia effectors have been characterised to date, but work is underway to identify effectors from the whole genome sequences and secretedproteins of V. inaequalis and V. pirina. Whole genome sequencing of Venturia inaequalis and V. pirina has revealed predicted proteins with some sequencesimilarity to AvrLm6, a Leptosphaeria maculans effector that triggers resistance in Rlm6 canola. The mechanism of action of AvrLm6 is unknown. Untilrecently, AvrLm6 was thought to be unique to L. maculans, with orthologues absent, even in closely related species. AvrLm6-like genes from Venturia sppwhose genomes are sequenced form large families containing up to 30 members. We have also identified orthologues in F. oxysporum (Fo5176) and C.higginsianum from public database searches. Gene expansions have also been observed for other effector-like genes in the Venturia genomes. TheAvrLm6-like predicted protein from V. inaequalis, with the highest sequence identity to AvrLm6, was unable to trigger a resistance response in Rlm6canola. However, this does not preclude the AvrLm6-like proteins from being functionally active in the Malus-Venturia pathosystem. Transcriptomeanalyses (RNA-seq) of in planta and in vitro samples of V. inaequalis have revealed that a number of AvrLm6-like genes are up-regulated during infection(compared to growth in vitro). These results were confirmed with qRT-PCR. The most highly up-regulated predicted protein, ALVi_149, was tagged withYFP. YFP expression was observed only in the sub-cuticular stromata (specialised, biotrophic infection structures). RNA silencing is currently underway todetermine the role of ALVi_149 in pathogenicity of V. inaequalis. The major question that remains is; what purpose do these genes serve for these diversefungi and what is driving the gene expansions in Venturia spp?250. Oömycetes Protein Array Project. Samantha Taylor 1 , Regina Hanlon 2 , Mandy Wilson 2 , Jean Peccoud 2 , Brett Tyler 1 . 1) Oregon State University,Corvallis, OR; 2) Virginia Tech, Blacksburg, VA.Oömycetes are eukaryotes that outwardly resemble fungi, but are related to brown and golden-brown algae. The most destructive oömycete genus isPhytophthora, with over 80 species that collectively attack a wide range of plant species, causing damage to crops that is estimated in billions of dollarsannually in the US. The goal of the Oömycetes Protein Array Project is to generate a collection of cloned proteins from 1440 predicted oömycete effectorsequences, to use Gateway® technology to facilitate the easy transfer of clones into expression vectors, and to make the resulting clones available to thescientific community for further research. When the project is over, the final collection should include 390 clones from P. sojae, 550 clones from P.infestans, 370 clones from P. ramorum, and 130 clones from H. arabidopsidis.251. Extensive chromosomal reshuffling drives evolution of virulence in an asexual pathogen. Ronnie de Jonge 1,2 , Melvin Bolton 3 , Anja Kombrink 1 , KosteYadeta 1 , Grardy van den Berg 1 , Bart Thomma 1 . 1) Laboratory of Phytopathology, Wageningen University, Droevendaalsesteeg 1, 6708 PB Wageningen, TheNetherlands; 2) VIB Department of Plant Systems Biology, Ghent University, Bioinformatics and Evolutionary Genomics Division, Technologiepark 927, B-9052 Gent, Belgium; 3) United States Department of Agriculture, Agricultural Research Service, Northern Crop Science Laboratory, Fargo, ND 58102-2765,United States.Sexual recombination drives genetic diversity in eukaryotic genomes, and fosters adaptation to novel environmental challenges. Although strictly asexualmicroorganisms are often considered as evolutionary dead ends, they comprise many devastating plant pathogens. Presently, it remains unknown howsuch asexual pathogens generate the genetic variation that is required for quick adaptation and evolution in the arms race with their hosts. Here we showthat extensive chromosomal rearrangements in the strictly asexual plant pathogenic fungus Verticillium dahliae establish highly dynamic ‘plastic’ genomicregions that act as a source for genetic variation to mediate aggressiveness. We show that these plastic regions are greatly enriched for in plantaexpressedeffector genes, encoding secreted proteins that enable host colonization including the previously identified race 1-specific effector Ave1 thatactivates Ve1-mediated resistance in tomato. The plastic regions occur at the flanks of chromosomal breakpoints and are enriched for repetitive sequenceelements, especially retrotransposons. Our results demonstrate that asexual pathogens may evolve by prompting chromosomal rearrangements, enabling182
FULL POSTER SESSION ABSTRACTSrapid development of novel effector genes. Likely, chromosomal reshuffling is a general mechanism for adaptation in asexually propagating organisms.252. Genomic census of transmembrane proteins of the marine fungus, Corollospora maritima. Derek Johnson, Joseph Spatafora. Botany and PlantPathology, Oregon State University, Corvallis, OR.The class Sordariomycetes (Ascomycota) presents a model phylogenetic system to study the genomic evolution of marine fungi, as there have been atleast four major independent transitions from terrestrial to marine environments. These marine fungi have adapted to an environment which requiresincreased control of the movement of water between the cell and the environment due to osmosis. Given this, the greatest adaptive pressure may befound working at the interface of the fungal cell with the environment in the form of transmembrane proteins and in biochemical pathways dealing inosmoregulation. We have initiated a comparative, phylogenomic study of the independent lineages of marine Sordariomycetes with the goal ofdetermining what pathways have been modified in the transition to the marine environment. Here we present preliminary data of the draft genome of themarine fungus Corollospora maritima, which is a member of the largest family of marine fungi, Halospheriaceae (Microascales). The draft genome of C.maritima is similar to other Sordariomycetes (37 MB, 10269 predicted gene models) but is characterized by an increased number of transmembraneproteins; both in raw number (2017), and as a percentage of protein coding genes (19.64%), than non-marine members of the Sordariomycetes. Thus, it ishypothesized that C. maritima has expanded osmoregulatory protein families and adapted novel transmembrane proteins as a consequence of thetransition to the marine environment. Transmembrane proteins belonging to C. maritima along with select species of fungi and Eukaryotes were predictedvia hidden markov modeling using the program TMHMM and clustered into orthologous groups using Ortho-MCL. Putative protein identities (e.g.,aquaporins, aquaglyceroporins, osmosensors and the sodium efflux ENA ATPases) were assigned to each cluster using the BLAST tool comparingorthologous protein cluster identities to proteins of the model organisms Neurospora crassa and Saccharomyces cerevisiae. Expansions and contractionsof transmembrane proteins will be presented in a phylogenetic context, and more complex patterns of evolution, such as more ancient lineage sorting vs.lineage specific expansions, will be tested for each orthologous group of proteins using gene tree/species tree reconciliation analyses.253. <strong>Fungal</strong> Calcium Signaling Database (FCSD). Venkatesh Moktali, Bongsoo Park, Seogchan Kang. Penn State University, University Park, PA 16802, USA.Calcium probably is one of the most versatile elements in biological systems. It serves as a pivotal signal in controlling diverse cellular and developmentalprocesses to ensure the healthy functioning of every organism ranging from microbes to humans. The mechanism of translating external stimuli to specificcellular and developmental responses via changes in calcium ions plays an essential role in the plant-microbe and microbe-environmental interactions.Accordingly, many genes of the calcium-signaling pathway have been found to be virulence factors of fungal pathogens. How this simple and ubiquitousion has evolved to control so many processes is one of the central questions in biology with many practical implications. Rapid advances in genomesequencing of many fungal and oomycete species have uncovered conserved core calcium signaling genes, as well as lineage-specific features. To supportsystematic studies on this evolutionary variability in fungi and oomycetes and the functional roles of individual genes, we built the <strong>Fungal</strong> Calcium SignalingDatabase (FCSD; http://fcsd.ifungi.org/), an online platform that categorizes and annotates key calcium signaling proteins from more than 120 publishedfungal and oomycete genomes. The database also archives experimental results from studies on mutants of calcium signaling genes and resulting calciumsignatures in both video and picture formats. The calcium signaling genes in FCSD are divided into five major groups namely, calcium-permeable channels,calcium pumps, calcium exchanger/antiporter, calcium signaling regulators, and calcium-binding proteins. Comparison of calcium signaling machineriesbetween fungi and oomycetes has been conducted to identify evolutionary changes that have shaped up this signaling pathway in these kingdoms. TheFCSD will greatly support the fungal community in studying and understanding calcium signaling.254. Evolutionary genomic analysis of cytochrome P450 proteins in the subphyla Pezizomycotina. Venkatesh Moktali, Seogchan Kang. The PennsylvaniaState University, University Park, PA 16802.The subphylum Pezizomycotina presents a vast diversity of ecological niches and biochemical processes observed in fungal subphyla. Changes inmembers of the cytochrome P450 (CYP) superfamily appear to have played key roles in fungal niche adaption and evolution. Availability of genomic datafrom many species in this subphylum has enabled comprehensive phylogenomic studies to understand the taxon-specific genetic changes that potentiallyunderpin the observed functional and ecological diversity. CYPs from 53 Pezizomycotina species were analyzed to study the gene birth and death patternsat the genus level. This analysis revealed niche- and class-specific CYP family expansions and contractions. Putative metabolic functions were assigned toindividual CYPs in each species based on sequence similarity to functionally characterized CYP proteins. Also, pathogenic Pezizomycotina fungi weredivided into three classes (hemibiotrophs, obligate biotrophs and necrotrophs) to identify CYP family expansions and innovations potentially associatedwith these classes. Large losses in CYP families were observed among obligate biotrophs whereas hemibiotrophs and necrotrophs showed gene gains aswell as functional innovation in the form of species-specific CYP families. Examination of the classes/divisions within Pezizomycotina suggested a numberof independent losses and gains in CYP families. These findings shall be presented in the poster.255. Uncovering the evolutionary pressures shaping the Glomeromycota-Glomeribacter endosymbiosis. Stephen J. Mondo, Teresa E. Pawlowska. PlantPathology, Cornell University, Ithaca, NY.Many eukaryotes interact with heritable endobacteria to satisfy diverse metabolic needs. Of the characterized fungal-bacterial endosymbioses, theassociation between Gigasporaceae (Glomeromycota) and Ca. Glomeribacter is one of the best described. Glomeribacter is a member of the Burkholderialineage of b-proteobacteria, and was shown previously to represent one of the few cases of an ancient, long-term non-essential endosymbiont. In order tofurther explore what adaptations have taken place to shape this unique bacterial lifestyle, we have sequenced three Glomeribacter genomes anddeveloped a computational pipeline to compare across bacteria engaging in different lifestyles using genome wide patterns of mutation accumulation. Weused PAML to identify gene orthologs that exhibited both over-accumulation and under-accumulation of amino acid substitutions and then used thesedata to compare across taxa at the level of functional gene categories. We found that bacteria can be grouped by lifestyle using this approach.Glomeribacter, as expected, appears most similar to other potentially long-term non-essential endosymbionts. Therefore, we were able to exploit thedifferences in mutation accumulation patterns between these taxa to identify processes, which may be relevant within the particular interaction betweenGlomeribacter and its host. While several of these processes, including vitamin synthesis and amino acid transport, have been identified previously, weadditionally discovered features related to lipid biosynthesis and energy metabolism to be of potential importance for this symbiosis. Interestingly, genesexhibiting an under-accumulation of nonsynonymous substitutions (indicative of purifying selection) in Glomeribacter tend to be involved inrecombination, cell division, and ribosome maintenance. While these processes are typically fast evolving in endosymbiotic organisms, they may representfeatures that increase the stability of Glomeribacter in their fungal host population and increase their resilience to genetic drift. We speculate that theseprocesses are unique to the Glomeribacter-Glomeromycota symbiosis and could partially explain why Glomeribacter has been successful as a nonessentialendosymbiont for over 400 million years.<strong>27th</strong> <strong>Fungal</strong> <strong>Genetics</strong> <strong>Conference</strong> | 183
- Page 1:
Asilomar Conference GroundsMarch 12
- Page 7 and 8:
SCHEDULE OF EVENTSFriday, March 157
- Page 10 and 11:
EXHIBITSThe following companies hav
- Page 12 and 13:
CONCURRENT SESSIONS SCHEDULESWednes
- Page 14:
CONCURRENT SESSIONS SCHEDULESWednes
- Page 17 and 18:
CONCURRENT SESSIONS SCHEDULESThursd
- Page 19:
CONCURRENT SESSIONS SCHEDULESFriday
- Page 22 and 23:
CONCURRENT SESSIONS SCHEDULESSaturd
- Page 24:
CONCURRENT SESSIONS SCHEDULESSaturd
- Page 27 and 28:
PLENARY SESSION ABSTRACTSThursday,
- Page 29 and 30:
PLENARY SESSION ABSTRACTSFriday, Ma
- Page 31 and 32:
PLENARY SESSION ABSTRACTSSaturday,
- Page 33 and 34:
CONCURRENT SESSION ABSTRACTSWednesd
- Page 35 and 36:
CONCURRENT SESSION ABSTRACTSUnravel
- Page 37 and 38:
CONCURRENT SESSION ABSTRACTSSynergi
- Page 39 and 40:
CONCURRENT SESSION ABSTRACTSWednesd
- Page 41 and 42:
CONCURRENT SESSION ABSTRACTSWednesd
- Page 43 and 44:
CONCURRENT SESSION ABSTRACTSWednesd
- Page 45 and 46:
CONCURRENT SESSION ABSTRACTSA draft
- Page 47 and 48:
CONCURRENT SESSION ABSTRACTSRegulat
- Page 49 and 50:
CONCURRENT SESSION ABSTRACTSWednesd
- Page 51 and 52:
CONCURRENT SESSION ABSTRACTSThursda
- Page 53 and 54:
CONCURRENT SESSION ABSTRACTSThursda
- Page 55 and 56:
CONCURRENT SESSION ABSTRACTSThursda
- Page 57 and 58:
CONCURRENT SESSION ABSTRACTSThursda
- Page 59 and 60:
CONCURRENT SESSION ABSTRACTSThursda
- Page 61 and 62:
CONCURRENT SESSION ABSTRACTSThe mut
- Page 63 and 64:
CONCURRENT SESSION ABSTRACTSInnate
- Page 65 and 66:
CONCURRENT SESSION ABSTRACTSThursda
- Page 67 and 68:
CONCURRENT SESSION ABSTRACTSGenome-
- Page 69 and 70:
CONCURRENT SESSION ABSTRACTSIdentif
- Page 71 and 72:
CONCURRENT SESSION ABSTRACTSFriday,
- Page 73 and 74:
CONCURRENT SESSION ABSTRACTSFriday,
- Page 75 and 76:
CONCURRENT SESSION ABSTRACTSThe Scl
- Page 77 and 78:
CONCURRENT SESSION ABSTRACTSThe rol
- Page 79 and 80:
CONCURRENT SESSION ABSTRACTSFriday,
- Page 81 and 82:
CONCURRENT SESSION ABSTRACTSCompari
- Page 83 and 84:
CONCURRENT SESSION ABSTRACTSNovel t
- Page 85 and 86:
CONCURRENT SESSION ABSTRACTSFriday,
- Page 87 and 88:
CONCURRENT SESSION ABSTRACTSEffect
- Page 89 and 90:
CONCURRENT SESSION ABSTRACTSCommon
- Page 91 and 92:
CONCURRENT SESSION ABSTRACTSSaturda
- Page 93 and 94:
CONCURRENT SESSION ABSTRACTSSeconda
- Page 95 and 96:
CONCURRENT SESSION ABSTRACTSSheddin
- Page 97 and 98:
CONCURRENT SESSION ABSTRACTSSaturda
- Page 99 and 100:
CONCURRENT SESSION ABSTRACTSSaturda
- Page 101 and 102:
CONCURRENT SESSION ABSTRACTSSaturda
- Page 103 and 104:
CONCURRENT SESSION ABSTRACTSprocess
- Page 105 and 106:
CONCURRENT SESSION ABSTRACTSSpecifi
- Page 107 and 108:
LISTING OF ALL POSTER ABSTRACTSBioc
- Page 109 and 110:
LISTING OF ALL POSTER ABSTRACTS81.
- Page 111 and 112:
LISTING OF ALL POSTER ABSTRACTS160.
- Page 113 and 114:
LISTING OF ALL POSTER ABSTRACTS239.
- Page 115 and 116:
LISTING OF ALL POSTER ABSTRACTS322.
- Page 117 and 118:
LISTING OF ALL POSTER ABSTRACTS401.
- Page 119 and 120:
LISTING OF ALL POSTER ABSTRACTSmedi
- Page 121 and 122:
LISTING OF ALL POSTER ABSTRACTS558.
- Page 123 and 124:
LISTING OF ALL POSTER ABSTRACTS640.
- Page 125 and 126:
LISTING OF ALL POSTER ABSTRACTS723.
- Page 127 and 128:
FULL POSTER SESSION ABSTRACTS5. Cha
- Page 129 and 130:
FULL POSTER SESSION ABSTRACTS13. In
- Page 131 and 132:
FULL POSTER SESSION ABSTRACTSbioche
- Page 133 and 134:
FULL POSTER SESSION ABSTRACTS30. Me
- Page 135 and 136: FULL POSTER SESSION ABSTRACTS38. Me
- Page 137 and 138: FULL POSTER SESSION ABSTRACTSidenti
- Page 139 and 140: FULL POSTER SESSION ABSTRACTSsecret
- Page 141 and 142: FULL POSTER SESSION ABSTRACTSinvolv
- Page 143 and 144: FULL POSTER SESSION ABSTRACTSdiploi
- Page 145 and 146: FULL POSTER SESSION ABSTRACTSSaccha
- Page 147 and 148: FULL POSTER SESSION ABSTRACTSresist
- Page 149 and 150: FULL POSTER SESSION ABSTRACTS96. Ce
- Page 151 and 152: FULL POSTER SESSION ABSTRACTS104. M
- Page 153 and 154: FULL POSTER SESSION ABSTRACTScan ex
- Page 155 and 156: FULL POSTER SESSION ABSTRACTSturgor
- Page 157 and 158: FULL POSTER SESSION ABSTRACTSlike p
- Page 159 and 160: FULL POSTER SESSION ABSTRACTSIndoor
- Page 161 and 162: FULL POSTER SESSION ABSTRACTSlength
- Page 163 and 164: FULL POSTER SESSION ABSTRACTSA scre
- Page 165 and 166: FULL POSTER SESSION ABSTRACTSthen q
- Page 167 and 168: FULL POSTER SESSION ABSTRACTS170. S
- Page 169 and 170: FULL POSTER SESSION ABSTRACTSof sup
- Page 171 and 172: FULL POSTER SESSION ABSTRACTSis fzo
- Page 173 and 174: FULL POSTER SESSION ABSTRACTSgrowth
- Page 175 and 176: FULL POSTER SESSION ABSTRACTSSeq da
- Page 177 and 178: FULL POSTER SESSION ABSTRACTS212. T
- Page 179 and 180: FULL POSTER SESSION ABSTRACTSCompar
- Page 181 and 182: FULL POSTER SESSION ABSTRACTSmore g
- Page 183 and 184: FULL POSTER SESSION ABSTRACTSmolecu
- Page 185: FULL POSTER SESSION ABSTRACTSunexpe
- Page 189 and 190: FULL POSTER SESSION ABSTRACTS260. T
- Page 191 and 192: FULL POSTER SESSION ABSTRACTSFusari
- Page 193 and 194: FULL POSTER SESSION ABSTRACTSScienc
- Page 195 and 196: FULL POSTER SESSION ABSTRACTS286. G
- Page 197 and 198: FULL POSTER SESSION ABSTRACTSincomp
- Page 199 and 200: FULL POSTER SESSION ABSTRACTSfound
- Page 201 and 202: FULL POSTER SESSION ABSTRACTS312. I
- Page 203 and 204: FULL POSTER SESSION ABSTRACTSall th
- Page 205 and 206: FULL POSTER SESSION ABSTRACTSPia La
- Page 207 and 208: FULL POSTER SESSION ABSTRACTS335. A
- Page 209 and 210: FULL POSTER SESSION ABSTRACTS342. F
- Page 211 and 212: FULL POSTER SESSION ABSTRACTSThis i
- Page 213 and 214: FULL POSTER SESSION ABSTRACTSJacobs
- Page 215 and 216: FULL POSTER SESSION ABSTRACTScalciu
- Page 217 and 218: FULL POSTER SESSION ABSTRACTSThe ab
- Page 219 and 220: FULL POSTER SESSION ABSTRACTSexpres
- Page 221 and 222: FULL POSTER SESSION ABSTRACTS394. F
- Page 223 and 224: FULL POSTER SESSION ABSTRACTS398. U
- Page 225 and 226: FULL POSTER SESSION ABSTRACTSthe id
- Page 227 and 228: FULL POSTER SESSION ABSTRACTS415. A
- Page 229 and 230: FULL POSTER SESSION ABSTRACTSAcuM b
- Page 231 and 232: FULL POSTER SESSION ABSTRACTSdiverg
- Page 233 and 234: FULL POSTER SESSION ABSTRACTSBck1 f
- Page 235 and 236: FULL POSTER SESSION ABSTRACTSin the
- Page 237 and 238:
FULL POSTER SESSION ABSTRACTS455. T
- Page 239 and 240:
FULL POSTER SESSION ABSTRACTSor hos
- Page 241 and 242:
FULL POSTER SESSION ABSTRACTSfragme
- Page 243 and 244:
FULL POSTER SESSION ABSTRACTSenhanc
- Page 245 and 246:
FULL POSTER SESSION ABSTRACTSassess
- Page 247 and 248:
FULL POSTER SESSION ABSTRACTSmating
- Page 249 and 250:
FULL POSTER SESSION ABSTRACTScommon
- Page 251 and 252:
FULL POSTER SESSION ABSTRACTSOne of
- Page 253 and 254:
FULL POSTER SESSION ABSTRACTScells
- Page 255 and 256:
FULL POSTER SESSION ABSTRACTSof Ave
- Page 257 and 258:
FULL POSTER SESSION ABSTRACTSascaro
- Page 259 and 260:
FULL POSTER SESSION ABSTRACTSis a n
- Page 261 and 262:
FULL POSTER SESSION ABSTRACTSand th
- Page 263 and 264:
FULL POSTER SESSION ABSTRACTSCiuffe
- Page 265 and 266:
FULL POSTER SESSION ABSTRACTSon oth
- Page 267 and 268:
FULL POSTER SESSION ABSTRACTScopies
- Page 269 and 270:
FULL POSTER SESSION ABSTRACTSChem.
- Page 271 and 272:
FULL POSTER SESSION ABSTRACTS593. C
- Page 273 and 274:
FULL POSTER SESSION ABSTRACTS601. P
- Page 275 and 276:
FULL POSTER SESSION ABSTRACTSE.elym
- Page 277 and 278:
FULL POSTER SESSION ABSTRACTSThe de
- Page 279 and 280:
FULL POSTER SESSION ABSTRACTSMicrob
- Page 281 and 282:
FULL POSTER SESSION ABSTRACTSchromo
- Page 283 and 284:
FULL POSTER SESSION ABSTRACTSmating
- Page 285 and 286:
FULL POSTER SESSION ABSTRACTSAt the
- Page 287 and 288:
FULL POSTER SESSION ABSTRACTSemerge
- Page 289 and 290:
FULL POSTER SESSION ABSTRACTS666. G
- Page 291 and 292:
FULL POSTER SESSION ABSTRACTSof che
- Page 293 and 294:
FULL POSTER SESSION ABSTRACTSthe lo
- Page 295 and 296:
FULL POSTER SESSION ABSTRACTSin the
- Page 297 and 298:
FULL POSTER SESSION ABSTRACTSpotent
- Page 299 and 300:
FULL POSTER SESSION ABSTRACTSpoint
- Page 301 and 302:
FULL POSTER SESSION ABSTRACTS716. p
- Page 303 and 304:
FULL POSTER SESSION ABSTRACTSnatura
- Page 305 and 306:
FULL POSTER SESSION ABSTRACTSelemen
- Page 307 and 308:
KEYWORD LISTABC proteins ..........
- Page 309 and 310:
KEYWORD LISThigh temperature growth
- Page 311 and 312:
AUTHOR LISTBolton, Melvin D. ......
- Page 313 and 314:
AUTHOR LISTFrancis, Martin ........
- Page 315 and 316:
AUTHOR LISTKawamoto, Susumu... 427,
- Page 317 and 318:
AUTHOR LISTNNadimi, Maryam ........
- Page 319 and 320:
AUTHOR LISTSenftleben, Dominik ....
- Page 321 and 322:
AUTHOR LISTYablonowski, Jacob .....
- Page 323 and 324:
LIST OF PARTICIPANTSLeslie G Beresf
- Page 325 and 326:
LIST OF PARTICIPANTSTim A DahlmannR
- Page 327 and 328:
LIST OF PARTICIPANTSIgor V Grigorie
- Page 329 and 330:
LIST OF PARTICIPANTSMasayuki KameiT
- Page 331 and 332:
LIST OF PARTICIPANTSGeorgiana MayUn
- Page 333 and 334:
LIST OF PARTICIPANTSNadia PontsINRA
- Page 335 and 336:
LIST OF PARTICIPANTSFrancis SmetUni
- Page 337 and 338:
LIST OF PARTICIPANTSAric E WiestUni