Plasmid Segregation: Birds of a Feather Try Not To Flock Together

Anand, Syam P.; Khan, Saleem A.

doi:10.1128/jb.01551-09

Cited by 6 publications

(5 citation statements)

References 17 publications

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“…Regarding the intracellular distribution of WH1(A31V)–mRFP amyloid particles, similar fluorescent spots have previously been described for multi‐copy plasmids lacking a partition system, when labelled with fluorescent protein reporters tightly bound to DNA (Pogliano et al ., 2001; Anand and Khan, 2010). However, such plasmid‐linked foci usually have better defined circular contours and are smaller in size than the WH(A31V) inclusions.…”

Section: Discussionmentioning

confidence: 99%

A DNA‐promoted amyloid proteinopathy in Escherichia coli

Fernández-Tresguerres¹,

Espina

Gasset-Rosa³

et al. 2010

Molecular Microbiology

161

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Section: Discussionmentioning

confidence: 99%

A DNA‐promoted amyloid proteinopathy in Escherichia coli

Fernández-Tresguerres¹,

Espina

Gasset-Rosa³

et al. 2010

Molecular Microbiology

161

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“…This would presumably lead to a mixup of plasmid replicates within the cell. Interestingly, based on this observation, Anand and Khan (2010) explicitly point to the “possibility of random assortment of daughter plasmids (sisters and nonsisters) during cell division”. In that case, our assumption of random segregation of wild-type and mutant plasmids would be reasonable.…”

Section: Discussionmentioning

confidence: 99%

Evolutionary rescue and drug resistance on multicopy plasmids

Santer

Uecker

2019

Preprint

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1Bacteria often carry "extra DNA" in form of plasmids in addition to their chro-2 mosome. Many plasmids have a copy number greater than one such that the genes 3 encoded on these plasmids are present in multiple copies per cell. This has evo-4 lutionary consequences by increasing the mutational target size, by prompting the 5 (transitory) co-occurrence of mutant and wild-type alleles within the same cell, and 6 by allowing for gene dosage effects. We develop and analyze a mathematical model for 7 bacterial adaptation to harsh environmental change if adaptation is driven by benefi-8 cial alleles on multicopy plasmids. Successful adaptation depends on the availability 9 of advantageous alleles and on their establishment probability. The establishment 10 process involves the segregation of mutant and wild-type plasmids to the two daugh-11 ter cells, allowing for the emergence of mutant-homozygous cells over the course of 12 several generations. To model this process, we use the theory of multi-type branch-13 ing processes, where a type is defined by the genetic composition of the cell. Both 14 factors -the number of adaptive alleles and their establishment probability -depend 15 on the plasmid copy number, and they often do so antagonistically. We find that 16 in the interplay of various effects, a lower or higher copy number may maximize the 17 probability of evolutionary rescue. The decisive factor is the dominance relationship 18 between mutant and wild-type plasmids and potential gene dosage effects. Results 19 from a simple model of antibiotic degradation indicate that the optimal plasmid copy 20 number may depend on the specific environment encountered by the population. 21 157 vidual establishes a permanent lineage of offspring. We provide an expression for p hom est in 158 Eq. (A.6). 159 Mathematical approach 160Whether the bacterial population successfully adapts or goes extinct depends on two factors: 161 the mutational supply and the establishment probability of the resistance mutation once 162

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“…In this work, the involvement of the host is strengthened by the finding that partition-defective mutants of IncC2 are also toxicity-defective. In addition, localization studies have revealed that RK2 is highly mobile in the absence of a partitioning system, but the plasmids become fixed to sites at the quarter positions of the cell in the presence of partitioning proteins (Anand and Khan, 2010; Derman et al, 2008). One interpretation is that a host factor anchors RK2 to a specific site(s) in the cell.…”

Section: Discussionmentioning

confidence: 99%

Different phenotypes of Walker-like A box mutants of ParA homolog IncC of broad-host-range IncP plasmids

Siddique

Figurski

2012

Plasmid

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The promiscuous IncPα plasmids RK2 and R995 encode a broad-host-range partition system, whose essential components include the incC and korB genes and a DNA site (OB) to which the korB product binds. IncC2, the smaller of the two incC products, is sufficient for stabilization of R995ΔincC. It is a member of the type Ia ParA family of partition ATPases. To better understand the role of ATP in partition, we constructed three alanine-substitution mutants of IncC2. Each mutation changed a different residue of the Walker-like ATP-binding and hydrolysis motif, including a lysine (K10) conserved solely among members of the ParA and MinD families. All three IncC2 mutants were defective in plasmid partition, but they differed from one another in other respects. The IncC2 T16A mutant, predicted to be defective in Mg2+ coordination, was severely impaired in all activities tested. IncC2 K10A, predicted to be defective in ATP hydrolysis, mediated enhanced incompatibility with R995 derivatives. IncC2 K15A, predicted to be defective in ATP binding, exhibited two distinct incompatibility properties depending on the genotype of the target plasmid. When in trans to plasmids carrying a complementable incC deletion, IncC2 K15A caused dramatic plasmid loss, even at low levels of expression. In trans to wild-type R995 or to R995ΔincC carrying a functional P1 partition system, IncC2 K15A-mediated incompatibility was significantly less than that caused by wild-type IncC2. All three Walker-like A box mutants were also defective for the host toxicity that normally results from co-overexpression of incC and korB. The phenotypes of the mutants support a model in which nucleotide hydrolysis is required for separation of paired plasmid complexes and possible interaction with a host factor.

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Plasmid Segregation: Birds of a Feather Try Not To Flock Together

Cited by 6 publications

References 17 publications

A DNA‐promoted amyloid proteinopathy in Escherichia coli

A DNA‐promoted amyloid proteinopathy in Escherichia coli

Evolutionary rescue and drug resistance on multicopy plasmids

Different phenotypes of Walker-like A box mutants of ParA homolog IncC of broad-host-range IncP plasmids

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