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Heather Maughan

Publications and source records attributed to Heather Maughan.

8 recordsLinked to original sources
PubMed2006

The loss of adaptive plasticity during long periods of environmental stasis.

Adaptive plasticity allows populations to adjust rapidly to environmental change. If this is useful only rarely, plasticity may undergo mutational degradation and be lost from a population. We consider a population of constant size N undergoing loss of plasticity at functional mutation rate m and with selective advantage s associated with loss. Environmental change events occur at rate theta per generation, killing all individuals that lack plasticity. The expected time until loss of plasticity in a fluctuating environment is always at least tau, the expected time until loss of plasticity in a static environment. When mN > 1 and N theta >> 1, we find that plasticity will be maintained for an average of at least 10(8) generations in a single population, provided tau > 18/theta. In a metapopulation, plasticity is retained under the more lenient condition tau > 1.3/theta, irrespective of mN, for a modest number of demes. We calculate both exact and approximate solutions for tau and find that it is linearly dependent only on the logarithm of N, and so, surprisingly, both the population size and the number of demes in the metapopulation make little difference to the retention of plasticity. Instead, tau is dominated by the term 1/(m+s/2).

Adaptation, Biological↗
PubMed2006

Mutations leading to loss of sporulation ability in Bacillus subtilis are sufficiently frequent to favor genetic canalization.

We measured the rate of mutations impairing sporulation ability in Bacillus subtilis as 0.003 in a mutator population, following 6000 generations of strong selection for sporulation that have previously been described. This means that the product of the population size and the functional mutation rate is approximately 10(5), well within the parameter range for which genetic canalization of sporulation ability is expected.

Bacillus subtilis↗
PubMed2006

The population genetics of phenotypic deterioration in experimental populations of Bacillus subtilis.

Although many examples of trait loss exist in nature, the underlying population genetic mechanism responsible for the loss is usually unknown. Selective or neutral processes can result in the deterioration of a trait, and often one of these is inferred based on indirect evidence. Furthermore, selective pressures that are unique to particular environments and the effect these might have on the population genetic cause of trait loss are not well understood. Here we describe an experimental evolution system where two different environments were used for addressing the population genetic cause of trait loss throughout evolutionary time. We found that growth in minimal medium (i.e., prototrophy) was lost in all populations regardless of the experimental environment and that the pattern of trait loss in one environment was due to selection, whereas in the other environment the cause remains inconclusive.

Bacillus subtilis↗
PubMed2004

Stochastic processes influence stationary-phase decisions in Bacillus subtilis.

It has recently been proposed that phenotypic variation in clonal populations of bacterial species results from intracellular "noise," i.e., random fluctuations in levels of cellular molecules, which would be predicted to be insensitive to selective pressure. To test this notion, we propagated five populations of Bacillus subtilis for 5,000 generations with selection for one phenotype: the decision to sporulate. In support of the noise hypothesis, we report that none of the populations responded to selection by improving their efficiency of sporulation, indicating that intracellular noise is independent of heritable genotype.

Bacillus subtilis↗
PubMed2004

Novel rpoB mutations conferring rifampin resistance on Bacillus subtilis: global effects on growth, competence, sporulation, and germination.

Previously, spontaneous rifampin resistance mutations were isolated in cluster I of the rpoB gene, resulting in amino acid replacements (Q469R, H482R, H482Y, or S487L) in the Bacillus subtilis RNA polymerase beta subunit (W. L. Nicholson and H. Maughan, J. Bacteriol. 184:4936-4940, 2002). In this study, each amino acid change in the beta subunit was observed to result in its own unique spectrum of effects on growth and various developmental events, including sporulation, germination, and competence for transformation. The results thus establish the important role played by the RNA polymerase beta subunit, not only in the catalytic aspect of transcription, but also in the regulation of major developmental events in B. subtilis.

Alleles↗
PubMed2003

Molecular correlates of genes exhibiting RNAi phenotypes in Caenorhabditis elegans.

Understanding genome-wide links between genotype and phenotype has generally been difficult due to both the complexity of phenotypes, and until recently, inaccessibility to large numbers of genes that might underlie a trait. To address this issue, we establish the association between particular RNAi phenotypes in Caenorhabditis elegans and sequence characteristics of the corresponding proteins and DNA. We find that genes showing RNAi phenotypes are long and highly expressed with little noncoding DNA and high rates of synonymous site substitution (KS). In addition, genes conferring RNAi phenotypes have significantly lower rates of nonsynonymous site substitution (KA). Collectively, these sequence features explain nearly 20% of the difference between the sets of loci that display or lack a RNAi-mediated effect, and reflect aspects both of the RNAi mechanism and the biological function of the genes. For example, the particularly low rate of evolution of genes in the sterility RNAi phenotype class suggests a role of C. elegans life history in shaping these patterns of sequence and expression characteristics on phenotypes. This approach also allows prediction of a set of heretofore-uncharacterized loci for which we expect future RNAi studies to reveal phenotypic effects (i.e., false negatives in present screens).

Animals↗
PubMed2002

The spectrum of spontaneous rifampin resistance mutations in the rpoB gene of Bacillus subtilis 168 spores differs from that of vegetative cells and resembles that of Mycobacterium tuberculosis.

Mutations causing rifampin resistance in vegetative cells of Bacillus subtilis 168 have thus far been mapped to a rather restricted set of alterations at either Q469 or H482 within cluster I of the rpoB gene encoding the beta subunit of RNA polymerase. In this study, we demonstrated that spores of B. subtilis 168 exhibit a spectrum of spontaneous rifampin resistance mutations distinct from that of vegetative cells. In addition to the rpoB mutations Q469K, Q469R, and H482Y previously characterized in vegetative cells, we isolated a new mutation of rpoB, H482R, from vegetative cells. Additional new rifampin resistance mutations arising from spores were detected at A478N and most frequently at S487L. The S487L change is the predominant change found in rpoB mutations sequenced from rifampin-resistant clinical isolates of Mycobacterium tuberculosis. The observations are discussed in terms of the underlying differences of the DNA environment within dormant cells and vegetatively growing cells.

Amino Acid Sequence↗