Brave Genomes
Microbial Genome Plasticity in the Face of Environmental Challenge
- 1st Edition - February 25, 2025
- Imprint: Academic Press
- Author: Silvia Bulgheresi
- Language: English
- Paperback ISBN:9 7 8 - 0 - 4 4 3 - 1 8 7 8 9 - 6
- eBook ISBN:9 7 8 - 0 - 4 4 3 - 1 8 7 8 8 - 9
The role of environmentally triggered genetic and epigenetic changes in microbial adaptation and evolution is still not broadly appreciated. Brave Genomes: Microbial Genome Pl… Read more
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Request a sales quoteThe role of environmentally triggered genetic and epigenetic changes in microbial adaptation and evolution is still not broadly appreciated. Brave Genomes: Microbial Genome Plasticity in the Face of Environmental Challenge narrates how microorganisms cope with environmental changes including unanticipated ones. Although it does comprise eukaryotes, it focuses on bacteria and – whenever possible – on archaea.
Among the environmentally sensitive sources of genome plasticity, the book treats tandem repeats, mutagenic break repair, transcription-associated mutagenesis and transposable elements. Additionally, it deals with epigenetic mechanisms such as DNA methylation and regulatory RNA-based systems. These not only regulate the activity of mobile DNA, they can also synergize with it. In closing, symbiosis and genetic noise are also discussed as possible sources of phenotypic plasticity.
Brave Genomes emphasizes the role of the environment in generating genotypic and phenotypic diversity. This emerges, in turn, as the most efficient response to challenging conditions.
Among the environmentally sensitive sources of genome plasticity, the book treats tandem repeats, mutagenic break repair, transcription-associated mutagenesis and transposable elements. Additionally, it deals with epigenetic mechanisms such as DNA methylation and regulatory RNA-based systems. These not only regulate the activity of mobile DNA, they can also synergize with it. In closing, symbiosis and genetic noise are also discussed as possible sources of phenotypic plasticity.
Brave Genomes emphasizes the role of the environment in generating genotypic and phenotypic diversity. This emerges, in turn, as the most efficient response to challenging conditions.
- Compares environmentally sensitive genetic systems across the three kingdoms of life (bacteria, archaea, eukaryotes)
- Compares environmentally sensitive epigenetic systems across the three kingdoms of life
- Brings together insights of illustrious scientists including Josep Casadésus, Remus Dame, Cedric Feschotte, William Martin, Eva Jablonka, Eugen Koonin
- Microbial symbioses and genetic noise are also treated as potential sources of phenotypic plasticity and adaptability together with more traditional sources
- Familiarizes biologists with this discipline by using a colloquial style
Bachelor, Master and PhD students and scientists in microbiology, genetics, epigenetics, microbial symbioses, Bachelor, Master and PhD students and scientists in general biology and evolutionary biology
- Title of Book
- Cover image
- Title page
- Table of Contents
- Copyright
- Dedication
- Preface
- Acknowledgments
- About the cover image artist
- Epigraph
- Chapter 1. 15 DNA facts
- 1 Nuclein was discovered by Friedrich Miescher in 1869
- 2 DNA is built from four nucleotides
- 3 DNA is the carrier of genetic information
- 4 DNA is a twisted ladder
- 5 All known self-reproducing cellular organisms contain DNA
- 6 DNA is big
- 7 To fit into cells, DNA is condensed, packed, and folded many times
- 8 Every human shares 99.9% of DNA with every other human
- 9 Each of us is a genetic mosaic
- 10 Eukaryotic genomes contain from zero to hundreds of thousands of introns
- 11 Depending on where the DNA is stored, organisms are called prokaryotes or eukaryotes
- 12 Eukaryotic DNA is stored in the nucleus
- 13 It takes 8h for the largest human chromosome to double
- 14 DNA in every human cell gets damaged tens of thousands of times per day
- 15 DNA can be damaged by radiation and chemicals
- Chapter 2. DNA fun facts: Hypermutable DNA, mutagenic DNA break repair, and transcription-associated mutagenesis
- 1 Hypermutable DNA
- 1.1 What do I mean by tandem repeats?
- 1.2 Distribution of tandem repeats across species and within bacterial genomes
- 1.3 Molecular mechanisms underlying the hypermutability of tandem repeats
- 1.4 Factors influencing tandem repeat mutability
- 1.5 How tandem repeats may impact the phenotype of bacteria
- 1.5.1 Tandem repeats within lipopolysaccharide biosynthesis genes
- 1.5.2 Tandem repeats within adhesin genes and alike
- 1.5.3 Tandem repeats within genes involved in restriction-modification
- 1.5.4 Tandem repeats within stress response genes
- 1.6 Tandem repeats and bacterial evolution
- 2 Mutagenic break repair: From bad to worse
- 2.1 Mutagenic break repair in bacteria
- 2.2 When it rains on the wet: Localization of mutations caused by mutagenic break repair
- 2.3 Nothing ventured, nothing gained: Gambler cells
- 2.4 Mutability and metabolism
- 2.5 Regulated mutagenesis in yeast
- 2.6 Mutagenic break repair and evolution
- 3 Transcription-associated mutagenesis: You cannot break a bike if you don't use a bike
- 3.1 Mechanisms underlying transcription-associated mutagenesis in bacteria
- 3.2 Consequences of transcription-associated mutagenesis in bacteria: Strand-related bias in the accumulation of mutations
- 3.3 Consequences of transcription-associated mutagenesis in bacteria: Codirectionality of DNA replication and transcription
- 3.4 Effects of stress on transcription-associated mutagenesis in bacteria
- 3.5 Transcription-associated mutagenesis in yeast
- 3.6 Effects of stress on transcription-associated mutagenesis in yeast
- 3.7 Beyond μ
- Chapter 3. On top of the DNA
- 1 DNA methylation
- 1.1 Bacterial DNA methylation as an immune system
- 1.2 Bacterial DNA methylation as an epigenetic system
- 1.3 Clocklike DNA methylation-dependent transcriptional control
- 1.3.1 Transcriptional control of DNA replication initiation in Escherichia coli
- 1.3.2 Transcriptional control of the outer membrane protein Ag43 in Escherichia coli
- 1.4 Switch-like DNA transcriptional control of multiple genes
- 1.5 Evolutionary aspects of bacterial DNA methylation
- 1.6 DNA methylation in eukaryotes
- 2 Nucleoid-associated proteins
- 2.1 Bacterial nucleoid-associated proteins: Three examples
- 2.1.1 Heat-unstable (HU) nucleoid protein, regulator of DNA flexibility
- 2.1.2 Histone-like nucleoid structuring (H-NS) protein, genome guardian and universal repressor
- 2.1.3 DNA-binding protein from starved cells (Dps), the DNA crystallizer
- 2.2 Nucleoid-associated proteins and the talking chromosome
- 2.3 Environmental regulation of chromosome folding
- 2.4 The evolving bacterial nucleoid
- 2.5 Archaeal chromatin
- 2.5.1 Archaeal histones
- 2.5.2 Archaeal histones and the talking archaeal chromosome
- 2.5.3 Archaeal nucleoid-associated proteins
- 3 The genome under the sway of RNA
- 3.1 Prokaryotic RNA-dependent systems
- 3.2 Eukaryotic RNA-dependent systems
- 3.3 Evolution of RNA interference and loss of clustered regularly interspaced short palindromic (CRISPR)-Cas immunity in eukaryotes
- 3.4 Bacterial regulatory RNAs
- 3.4.1 Bacterial cis-acting regulatory RNAs
- 3.4.2 Bacterial trans-acting regulatory RNAs
- 3.4.3 How bacterial trans-acting RNAs work
- 3.4.4 The matchmaking RNA chaperone Hfq
- 3.4.5 The CsrA system
- 4 On top of the top: Microbes as epigenetic inheritance systems
- 4.1 Microbes as modifiers of the host epigenome
- 4.2 Gut microbiota affecting mammalian DNA methylation
- 4.3 Gut microbiota as modifiers of mammalian histones
- 4.4 Gut microbiota as modifiers of mammalian regulatory RNA
- 4.5 And vice versa: Hosts as modifiers of microbial regulatory RNA
- 4.6 On top of the top: Microbes as epigenetic inheritance systems
- Chapter 4. DNA very fun facts
- 1 Basics of Transposons
- 1.1 How we classify transposons
- 1.2 Types of DNA transposons and RNA transposons
- 1.3 What transposons can actually do
- 1.4 What transposons can do to nearby genes when they stay where they are (cis-activity)
- 1.5 What transposons can do to host transcripts (in cis or in trans)
- 1.6 What transposon can do when they move
- 1.7 How to avoid the worst: Stopping transposons
- 1.7.1 DNA methylation
- 1.7.2 Regulatory RNA
- 1.7.3 Repressive histone modifications
- 1.7.4 ATP-dependent chromatin remodelers
- 1.7.5 Programmed DNA elimination
- 1.7.6 Silencing of the bacterial transposon Tn5 by riboregulation and DNA methylation
- 1.8 And yet they move
- 1.9 Smelling danger: Effect of stress on eukaryotic transposons
- 1.10 Smelling danger: Effect of stress on bacterial transposons
- 1.11 The pros and cons of stress-induced transposon activity
- 1.12 Where to? Domestic destinations
- 1.12.1 Transposons that integrate into gene-rich regions
- 1.12.2 Transposons that integrate into heterochromatin
- 1.12.3 Transposons that integrate at chromosome ends
- 1.12.4 Dispersed patterns of transposon integration
- 2 Going away for good: Horizontal transfer of transposons
- 2.1 Horizontal gene transfer between bacteria
- 2.2 Genomic islands
- 2.3 Integrative and conjugative elements
- 2.3.1 Activation of integrative and conjugative elements
- 2.3.2 Induction of integrative and conjugative elements during the SOS response
- 2.3.3 Induction of integrative and conjugative elements during the stationary phase
- 2.3.4 Induction by the phenotype conferred to the host
- 2.3.5 Induction through cell–cell signaling
- 2.3.6 Induction upon entry into a new host
- 2.4 Transposable phages
- 2.4.1 Transposable phage Mu and horizontal gene transfer
- 2.4.2 Beyond Mu: The Saltoviridae family
- 2.5 Horizontal transfer of transposons between bacteria and eukaryotes
- 2.6 Horizontal transfer of transposons between eukaryotes: How often?
- 2.7 Factors facilitating horizontal gene transfer of transposons between eukaryotes
- 3 Grand finale
- 3.1 How many transposons in a eukaryotic genome?
- 3.2 How many transposons in a prokaryotic genome?
- 3.3 Transposons and the origin of our placenta, or: Had we not been infected by a retrovirus, we would still be laying eggs
- 3.4 Transposons and animal adaptive immunity: No transposons, no antibodies
- 3.5 Transposons and prokaryotic adaptive immunity: No transposons, no clustered regularly interspaced short palindromic repeats (CRISPR)-Cas
- 3.6 Epigenetic systems and transposable elements: United they stand?
- Chapter 5. No two cells are alike
- 1 What I mean by molecular noise
- 2 Some genes are noisier than others
- 3 What controls genetic noise
- 3.1 Gene copy number
- 3.2 Promoter design
- 3.3 Chromatin structure
- 3.4 Posttranscriptional factors
- 4 As a source of phenotypic noise, genetic noise may affect fitness
- 5 Bacterial persisters: A case study for how chance can affect fitness
- 5.1 The role of chance in the formation of persisters
- 5.2 Persister formation during exponential growth
- 5.3 Persister formation during nutrient transitions
- 5.4 Persister formation during stress
- 6 Noise is evolvable
- 6.1 Positive selection for low phenotypic noise
- 6.2 Noise evolution under fully neutral selection
- 6.3 Positive selection for elevated noise
- 7 Molecular noise is good and bad (just like mobile DNA and pretty much everything else in life)
- Glossary
- Postface
- Index
- Edition: 1
- Published: February 25, 2025
- Imprint: Academic Press
- No. of pages: 332
- Language: English
- Paperback ISBN: 9780443187896
- eBook ISBN: 9780443187889
SB
Silvia Bulgheresi
Silvia Bulgheresi is Associate Professor in Environmental Cell Biology and independent researcher at the University of Vienna. Her research on the molecular mechanisms underlying symbiont growth, division and chromosome segregation challenged long-established bacterial cell biology tenets. Since 2008, she has been teaching environmental cell biology, microbial symbioses, as well as microbial genome plasticity to Bachelor, Master ad PhD students. It is in the effort of collecting the notes, thoughts and students’ questions that arose over two decades that this book was born.
Affiliations and expertise
Associate Professor in Environmental Cell Biology, Department of Functional and Evolutionary Ecology, University of Vienna, AustraliaRead Brave Genomes on ScienceDirect