Holger Brüggemann

Prof. Dr. Holger Brüggemann

Department of Biomedicine, Aarhus University, Skou Building, Høegh-Guldbergs Gade 10, 8000 Aarhus C, Denmark

Research Focus & Metrics

Academic Career Length

27Years (2000-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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3 October 2004 in Nature Genetics
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Journal Article
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CCChristel Cazalet
Christel Cazalet
CRChristophe Rusniok
Christophe Rusniok
HBHolger Bruggemann
Holger Bruggemann
NZNora Zidane
Nora Zidane
AMArnaud Magnier
Arnaud Magnier
CBCarmen Buchrieser
Carmen Buchrieser
Legionella pneumophila, the causative agent of Legionnaires' disease, replicates as an intracellular parasite of amoebae and persists in the environment as a free-living microbe. Here we have analyzed the complete genome sequences of L. pneumophila Paris (3,503,610 bp, 3,077 genes), an endemic strain that is predominant in France, and Lens (3,345,687 bp, 2,932 genes), an epidemic strain responsible for a major outbreak of disease in France. The L. pneumophila genomes show marked plasticity, with three different plasmids and with about 13% of the sequence differing between the two strains. Only strain Paris contains a type V secretion system, and its Lvh type IV secretion system is encoded by a 36-kb region that is either carried on a multicopy plasmid or integrated into the chromosome. Genetic mobility may enhance the versatility of L. pneumophila. Numerous genes encode eukaryotic-like proteins or motifs that are predicted to modulate host cell functions to the pathogen's advantage. The genome thus reflects the history and lifestyle of L. pneumophila, a human pathogen of macrophages that coevolved with fresh-water amoebae.

12 February 2008 in Proceedings of the National Academy of Sciences
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HSHenning Seedorf
Henning Seedorf
WFW. Florian Fricke
W. Florian Fricke
BVBirgit Veith
Birgit Veith
HBHolger Bruggemann
Holger Bruggemann
HLHeiko Liesegang
Heiko Liesegang
GGGerhard Gottschalk
Gerhard Gottschalk
Clostridium kluyveriis unique among the clostridia; it grows anaerobically on ethanol and acetate as sole energy sources. Fermentation products are butyrate, caproate, and H2. We report here the genome sequence ofC. kluyveri, which revealed new insights into the metabolic capabilities of this well studied organism. A membrane-bound energy-converting NADH:ferredoxin oxidoreductase (RnfCDGEAB) and a cytoplasmic butyryl-CoA dehydrogenase complex (Bcd/EtfAB) coupling the reduction of crotonyl-CoA to butyryl-CoA with the reduction of ferredoxin represent a new energy-conserving module in anaerobes. The genes for NAD-dependent ethanol dehydrogenase and NAD(P)-dependent acetaldehyde dehydrogenase are located next to genes for microcompartment proteins, suggesting that the two enzymes, which are isolated together in a macromolecular complex, form a carboxysome-like structure. Unique for a strict anaerobe,C. kluyveriharbors three sets of genes predicted to encode for polyketide/nonribosomal peptide synthetase hybrides and one set for a nonribosomal peptide synthetase. The latter is predicted to catalyze the synthesis of a new siderophore, which is formed under iron-deficient growth conditions.

30 July 2004 in Science
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HBHolger Bruggemann
Holger Bruggemann
AHAnke Henne
Anke Henne
FHFrank Hoster
Frank Hoster
HLHeiko Liesegang
Heiko Liesegang
AWArnim Wiezer
Arnim Wiezer
GGGerhard Gottschalk
Gerhard Gottschalk
Propionibacterium acnes is a major inhabitant of adult human skin, where it resides within sebaceous follicles, usually as a harmless commensal although it has been implicated in acne vulgaris formation. The entire genome sequence of this Gram-positive bacterium encodes 2333 putative genes and revealed numerous gene products involved in degrading host molecules, including sialidases, neuraminidases, endoglycoceramidases, lipases, and pore-forming factors. Surface-associated and other immunogenic factors have been identified, which might be involved in triggering acne inflammation and other P. acnes –associated diseases.

4 April 2004 in Nature Biotechnology
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AHAnke Henne
Anke Henne
HBHolger Bruggemann
Holger Bruggemann
CRCarsten Raasch
Carsten Raasch
AWArnim Wiezer
Arnim Wiezer
THThomas Hartsch
Thomas Hartsch
HFHans-Joachim Fritz
Hans-Joachim Fritz

22 August 2006 in Proceedings of the National Academy of Sciences
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EBElzbieta Brzuszkiewicz
Elzbieta Brzuszkiewicz
HBHolger Bruggemann
Holger Bruggemann
HLHeiko Liesegang
Heiko Liesegang
MEMelanie Emmerth
Melanie Emmerth
TÖTobias Ölschläger
Tobias Ölschläger
UDUlrich Dobrindt
Ulrich Dobrindt
Uropathogenic Escherichia coli (UPEC) strain 536 (O6:K15:H31) is one of the model organisms of extraintestinal pathogenic E. coli (ExPEC). To analyze this strain's genetic basis of urovirulence, we sequenced the entire genome and compared the data with the genome sequence of UPEC strain CFT073 (O6:K2:H1) and to the available genomes of nonpathogenic E. coli strain MG1655 (K-12) and enterohemorrhagic E. coli . The genome of strain 536 is ≈292 kb smaller than that of strain CFT073. Genomic differences between both UPEC are mainly restricted to large pathogenicity islands, parts of which are unique to strain 536 or CFT073. Genome comparison underlines that repeated insertions and deletions in certain parts of the genome contribute to genome evolution. Furthermore, 427 and 432 genes are only present in strain 536 or in both UPEC, respectively. The majority of the latter genes is encoded within smaller horizontally acquired DNA regions scattered all over the genome. Several of these genes are involved in increasing the pathogens' fitness and adaptability. Analysis of virulence-associated traits expressed in the two UPEC O6 strains, together with genome comparison, demonstrate the marked genetic and phenotypic variability among UPEC. The ability to accumulate and express a variety of virulence-associated genes distinguishes ExPEC from many commensals and forms the basis for the individual virulence potential of ExPEC. Accordingly, instead of a common virulence mechanism, different ways exist among ExPEC to cause disease.

27 January 2003 in Proceedings of the National Academy of Sciences
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Journal Article
Closed access
HBHolger Bruggemann
Holger Bruggemann
SBSebastian Bäumer
Sebastian Bäumer
WFWolfgang Florian Fricke
Wolfgang Florian Fricke
AWArnim Wiezer
Arnim Wiezer
HLHeiko Liesegang
Heiko Liesegang
GGGerhard Gottschalk
Gerhard Gottschalk
Tetanus disease is one of the most dramatic and globally prevalent diseases of humans and vertebrate animals, and has been reported for over 24 centuries. The manifestation of the disease, spastic paralysis, is caused by the second most poisonous substance known, the tetanus toxin, with a human lethal dose of ≈1 ng/kg. Fortunately, this disease is successfully controlled through immunization with tetanus toxoid; nevertheless, according to the World Health Organization, an estimated 400,000 cases still occur each year, mainly of neonatal tetanus. The causative agent of tetanus disease is Clostridium tetani , an anaerobic spore-forming bacterium, whose natural habitat is soil, dust, and intestinal tracts of various animals. Here we report the complete genome sequence of toxigenic C . tetani E88, a variant of strain Massachusetts. The genome consists of a 2,799,250-bp chromosome encoding 2,372 ORFs. The tetanus toxin and a collagenase are encoded on a 74,082-bp plasmid, containing 61 ORFs. Additional virulence-related factors could be identified, such as an array of surface-layer and adhesion proteins (35 ORFs), some of them unique to C . tetani . Comparative genomics with the genomes of Clostridium perfringens , the causative agent of gas gangrene, and Clostridium acetobutylicum , a nonpathogenic solvent producer, revealed a remarkable capacity of C . tetani : The organism can rely on an extensive sodium ion bioenergetics. Additional candidate genes involved in the establishment and maintenance of a pathogenic lifestyle of C . tetani are presented.