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PubMed1998

Adaptive mutagenesis: a process that generates almost exclusively beneficial mutations.

Adaptive mutations are spontaneous mutations that occur in microorganisms during periods of prolonged stress in non-dividing or very slowly dividing populations and that are specific to the environmental challenge that causes that stress. This article reviews the literature on adaptive mutagenesis since 1993. The evidence that adaptive mutagenesis is both real and general is considered. The most widely used system for studying adaptive mutagenesis, reversion of an F'-borne lacI33 allele, is shown to be a special case that reflects more about F-plasmid biology than about adaptive mutagenesis in general. New evidence demonstrating that adaptive mutagenesis is, indeed, specific is discussed. A variety of genes whose products affect adaptive mutagenesis are discussed. A model to explain that specificity and new evidence in support of that model are considered, as are potential roles of adaptive mutagenesis in evolution and practical aspects of adaptive mutagenesis.

Adaptation, Physiological↗
PubMed1998

[Cellular adaptation and cancerogenesis].

The paper describes the main adaptive mechanisms involved in the carcinogenic process. As a result of the action of carcinogenic agents (physical, chemical, biological), and in relation to the functional status of the affected cells, a number of systems are triggered off: detoxification and conjugation systems, the metabolisation of the said agents, DNA repairing enzymes, increased shock proteins (HSP), the induction of clonal proliferation. All these systems are valuable to the survival of the body and the species and culminate in the apoptosis of damaged cells as the last attempt at adaptation of a social kind for the good of the body. When these compensation mechanisms prove ineffective, imprecise or are exceeded by cell adaptive capacity, the resulting structural and functional alterations trigger off (induction) a very long process which often lasts between one and two thirds of the body's life, in various stages, multistep and multifactorial: this neoplastic transformation leads to a purposeless, egoistic, anarchic proliferation of cells which wish to survive at all costs, even to the detriment of the body of which they form part. Following the exhaustion of cell adaptive defences, there is an accumulation of additional genetic alterations (promotion and progression), the cells become manifestly neoplastic and continue their egoistic adaptation, according to the laws of natural selection: the cells which survive are those which adapt best to the hostile environment of the host's body, which are unaffected by proliferation control mechanisms (contact inhibition, differentiation factors, apoptosis, etc.), which make the best of the growth factors present in their microenvironment, which accomplish the so-called decathlon of the metastatization process, namely acquiring new capacities which can overcome the basal membrane, invade tissues to which they are attracted and continue to proliferate. Manifestly neoplastic cells become not self at a later stage, managing to escape the immune system using various adaptive mechanisms which induce immune tolerance/anergy. From this point of view, cancer may be regarded as an incidental factor in the host's cell adaptation processes; the latter are much more important from a biological point of view and their absence is incompatible with life: cancer might therefore be regarded as a cell adaptation pathology.

Adaptation, Physiological↗
PubMed1999

High altitude living: genetic and environmental adaptation.

High altitude (HA) living produces physiological changes for adaptation to chronic hypobaric-hypoxemic conditions. Although much is known about these physiologic adaptations, no clear separation has been made regarding what is "native" or "genetic" adaptation and what is "acquired." In this review, we describe the genetic vs. acquired adaptation and only include studies performed in a population native to HA and not in an acclimatized population or trekkers. The changes encountered in animals and humans living at HA in terms of hematology, muscular, respiratory, cerebral, cardiovascular, hormonal, fluid and electrolytes and reproduction, strongly suggest that genetics play a very important role in HA adaptation. Unfortunately, the characteristic physiology of HA natives has not been systematically defined to established specific measurable parameters of adaptation in comparison to the acquired ambient adaptation of the non-native population. Once the parameters are established, we can compare non-native populations exposed to HA that must emulate the HA physiology for a definite adaptation to be present. With measurable parameters, especially in the management of fluids and electrolytes, we can define how long it will take for a sea level native to adapt to an HA altitude. Until these studies are performed, speculation will continue and no rational medical intervention can be offered to HA newcomers who may experience HA difficulties.

Adaptation, Physiological↗
PubMed2025

Constraints in temperature adaptation reinforce differences in thermal niche between mesophilic and psychrotolerant Bacillus cereus group species.

Experimental evolution has demonstrated that mesophilic microbes readily adapt to increases in temperature. However, many microbes are psychrotolerant and resistant to cold, which is associated with physiological specializations, suggesting constraints in thermal adaptation. We hypothesized that constraints would limit adaption differently in a mesophilic species (Bacillus thuringiensis) compared with its psychrotolerant relative B. mycoides-with adaptation at cooler temperatures and adaptation at higher temperatures being constrained in each species, respectively. To test this hypothesis, we imposed 140 generations of selection at temperatures at and below the optimum for productivity for both species. The fitness and thermal performance of evolved bacteria showed ancestral thermal niche plays a role in thermal adaptation over this time scale, in support of our hypothesis of adaptive constraints. Temperature-dependent trade-offs appeared common in B. mycoides, with fitness gains associated with decreases in operational niche width; fitness gains at one temperature caused a decrease in the range of temperatures that the bacterium showed appreciable growth. Genome resequencing showed that variation in mutation supply and selection strength could not explain temperature-dependent responses to selection. Importantly, metabolic theory only held true for mesophilic B. thuringiensis, showing abundant but less studied psychrotolerant species could follow different adaptive trajectories.

Bacillus thuringiensis↗
PubMed2001

Driving in the future: temporal visuomotor adaptation and generalization.

Rapid and accurate visuomotor coordination requires tight spatial and temporal sensorimotor synchronization. The introduction of a sensorimotor or intersensory misalignment (either spatial or temporal) impairs performance on most tasks. For more than a century, it has been known that a few minutes of exposure to a spatial misalignment can induce a recalibration of sensorimotor spatial relationships, a phenomenon that may be referred to as spatial visuomotor adaptation. Here, we use a high-fidelity driving simulator to demonstrate that the sensorimotor system can adapt to temporal misalignments on very complex tasks, a phenomenon that we refer to as temporal visuomotor adaptation. We demonstrate that adapting on a single street produces an adaptive state that generalizes to other streets. This shows that temporal visuomotor adaptation is not specific to a single visuomotor transformation, but generalizes across a class of transformations. Temporal visuomotor adaptation is strikingly parallel to spatial visuomotor adaptation, and has strong implications for the understanding of visuomotor coordination and intersensory integration.

Adaptation, Ocular↗
PubMed1987

Glomerular ultrastructure of the trout, Salmo gairdneri: effects of angiotensin II and adaptation to seawater.

The effect of angiotensin infusion on the glomerular ultrastructure of freshwater- and seawater-adapted rainbow trout. Salmo gairdneri, has been examined by scanning and transmission electron microscopy. Adaptation of trout to seawater resulted in epithelial podocyte flattening, primary process broadening and apparent loss of foot processes in almost all glomeruli, features which were uncommon in freshwater-adapted trout. Similar changes were induced by infusion of freshwater-adapted animals with angiotensin, suggesting that the renin-angiotensin system plays a role in the modification of glomerular epithelial ultrastructure. Adaptation of trout to seawater also reduced glomerular diameter, but infusion of freshwater-adapted animals with angiotensin did not mirror this effect. Infusion of angiotensin into seawater-adapted animals increased the overall thickness of glomerular basement membrane by increasing the lamina rara interna and lamina densa. This did not occur when freshwater-adapted fish were either infused with angiotensin or adapted to seawater. These findings suggest that other humoral systems are involved in the control of glomerular diameter and basement membrane thickness as part of an integrated response to increased environmental salinity.

Acclimatization↗
PubMed1991

Visually-induced adaptive plasticity in the human vestibulo-ocular reflex.

The vestibulo-ocular reflex (VOR) is under adaptive control which corrects VOR performance when visual-vestibular mismatch arises during head movements. However, the dynamic characteristics of VOR adaptive plasticity remain controversial. In this study, eye movements (coil technique) were recorded from normal human subjects during sinusoidal rotations in darkness before and after 8 h. of adaptation to 2X binocular lenses. The VOR was studied at 7 frequencies between 0.025 and 4.0 Hz at 50 degrees/s peak head velocity (less for 2.5-4 Hz). For 0.025 and 0.25 Hz, the VOR was tested at 4 peak head velocities between 50 and 300 degrees/s. Before 2X lens adaptation, VOR gain was around 0.9 at 2.5-4.0 Hz and dropped gradually with decreasing frequency to under 0.6 at 0.025 Hz. Phase showed a small lead at the highest frequencies which declined to 0 degree as frequency decreased to 0.5-0.25 Hz, but then rose to 14 degrees by 0.025 Hz. VOR gain was independent of head velocity in the range 50-300 degrees/s at both 0.025 and 0.25 Hz. However, Phase lead rose with increasing head velocity, more so at 0.025 than at 0.25 Hz. After 2X lens adaptation, gain rose across the frequency bandwidth. However, the proportional gain enhancement was frequency dependent; it was greatest at 0.025 Hz (44%), and declined with increasing frequency to reach a minimum at 4 Hz (19%). Phase lead increased after 2X lens adaptation at lower frequencies, but decreased at higher frequencies. New velocity-dependent gain nonlinearities also developed which were not present prior to adaptation; gain declined as peak head velocity increased from 50 to 300 degrees/s at both 0.025 (23% drop) and 0.25 Hz (15% drop). This may suggest an amplitude-dependent limitation in VOR adaptive plasticity. Results indicate both frequency and amplitude dependent nonlinearities in human VOR response dynamics before and after adaptive gain recalibration.

Acclimatization↗
PubMed1988

Neural correlates of motion after-effects in cat striate cortical neurones: monocular adaptation.

Motion after-effects were elicited from striate cortical cells in lightly-anaesthetized cats, by adapting with square-wave gratings or randomly textured fields drifting steadily and continuously in preferred or null directions. The time-course and recovery of responsiveness following adaptation were assessed with moving bars, gratings or textured fields. Results were compared with controls in which the adapting stimulus was replaced by a uniform field of identical mean luminance, and also assessed in relation to the strength and time course of adaptation. Within 30-60 s adaptation, firing declined to a steady-state. Induced after-effects were direction-specific, and manifest as a transitory depression in response to the direction of prior adaptation, recovering to control levels in 30-60 s. Maximal after-effects were induced by gratings of optimal drift velocity and spatial frequency. With rare exceptions after-effects were restricted to driven activity; no consistent effects on resting discharge were observed. The onset of adaptation, and the recovery period, were more rapid in simple cells, although after-effects of comparable strength were elicited from simple and from standard complex cells. Special complex cells, including many of the more profoundly texture-sensitive neurones in the cortex, were more resistant to adaptation. The results support the conclusion that psychophysically measured adaptation and induced motion after-effect phenomena reflect the known properties of cortical neurones.

Animals↗
PubMed1987

DNA base changes induced following in vivo exposure of unadapted, adapted or ada- Escherichia coli to N-methyl-N'-nitro-N-nitrosoguanidine.

The adaptive response is one of the major repair pathways in Escherichia coli that removes DNA alkylation damage. To investigate the role of the adaptive response in mutagenesis, the E. coli gpt forward mutation assay system was used to determine the mutation spectrum of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in MNNG-adapted and unadapted GP120 (wild-type) and unadapted PJ5 (ada-5) cells. We observed that 34/37 mutations in the unadapted GP120 cells, 38/40 mutations in the adapted GP120 cells, and 10/10 mutations in the PJ5 cells were GC----AT transitions. The remaining 3/37 mutations in the unadapted GP120 cells were large insertions. The remaining 2/40 mutations in the adapted GP120 cells were transversions with one a GC----CG and the other an AT----CG. A surrounding sequence specificity of mutagenesis was observed for the GC----AT transitions in both the unadapted (GP120 and PJ5) and adapted (GP120) cells, with 70% of the unadapted PJ5, 68% of the unadapted GP120, and 61% of the adapted GP120 mutations occurring at the middle G of the sequence 5'--GG(A or T)--3'. Both strains also displayed a statistically significant preference for mutagenesis at guanine bases in the non-transcribed strand. The overall distribution of mutated sites in the gpt gene in adapted and unadapted cells was similar, although the rate of mutations at certain sites appeared different. These minor differences could result from either non-uniform repair of alkylation damage at different sites on the DNA, or altered processing of the alkylated bases to mutations in the adapted state.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkylation↗
PubMedDate not supplied

Comparison of adaptive filtering in time-, transform- and frequency-domain: an electrogastrographic study.

Adaptive cancellation of motion artifacts in the electrogastrogram (EGG) is presented in this paper. The EGG is a surface measurement of gastric electrical activity. Like other noninvasive electrophysiological measurements, the EGG contains motion artifacts. A number of papers have been published on the adaptive cancellation of motion artifacts or interferences in biomedical signals. Adaptive filtering was performed in time domain in almost all of the previous publications. In this paper, however, three different sorts of adaptive filters were investigated and their efficiencies in cancellation of motion artifacts were compared with each other. These include time-domain, transform-domain, and frequency-domain adaptive filters. A series of simulations were conducted to investigate the performance of these adaptive filters in cancellation of respiratory and motion artifacts. The results show that the frequency-domain adaptive filter has superior performance over the time- and transform-domain adaptive filters in the cancellation of stationary respiratory artifacts in the EGG. Although results focus on the EGG, this paper provides useful information for adaptive filtering of other biomedical signals.

Algorithms↗
PubMed2002

After-effects of visuo-manual adaptation to prisms on body posture in normal subjects.

Postural equilibrium is known to be controlled by sensorimotor reflexes and automatic control loops but also depends on high-level body representation in space, probably implicating the right temporoparietal cortex. Indeed, short-term prism adaptation to a 10 degrees rightward visual shift has been shown to reduce predominant postural imbalance in patients with right hemisphere damage, as it did for neglect symptoms. These effects are likely to be explained by a high level effect of prism adaptation on body and space representation, rather than by a sensorimotor effect. Cognitive after-effects of prism adaptation to a leftward visual shift, suggesting neglect-like symptoms, have also recently been shown in normal subjects on line bisection tasks. In the present study, we investigated the effect of wedge prism adaptation on postural control in normal subjects. Two groups of seven healthy subjects were either adapted to a leftward or a rightward visual shift. Results showed that our procedure induced changes in lateral postural control in normal subjects. Furthermore, this lateral postural after-effect was dependent on direction of prism adaptation. Indeed, only adaptation to a leftward visual shift induced significant rightward postural bias in normal subjects. The rightward postural lateral displacement was negatively correlated with the visual vertical. Both transfer and direction specific effect of visuo-manual adaptation to prisms on postural control suggest that effects of adaptation act more on high-level postural control linked to body representation in space or at least reveal close interaction between sensorimotor plasticity and body representation.

Adolescent↗
PubMed2000

The activity of primate ventrolateral thalamic neurones during motor adaptation.

Three monkeys were trained to perform stereotyped wrist movements to track a target (phase 1). Changing the gain between the wrist movement and visual display required the monkey to adapt its wrist movement. This adaptation consisted of progressive reduction of movement amplitude over a number of trials (phase 2) until a stereotyped movement accommodating the new gain was learned (phase 3). The experiment's aim was to investigate whether cerebellar thalamic neuronal discharge (ND) changed during motor adaptation and whether this change was related to scaling of kinematic parameters or movement error. Extracellular single-cell recordings were made from "wrist-related" neurones in the cerebellar thalamus (59) and the nucleus ventro-posterior lateralis caudalis (VPLc) (37) of each monkey while they performed the movement paradigm. Neurones were selected for further analysis (37/59 cerebellar thalamic and 23/37 VPLc) if phase-1 movements were stereotyped and motor adaptation occurred in phase 2 (according to statistical definitions). When the gain initially changed, there were positional errors in the form of overshoot. Adaptation to the new gain was achieved by a variety of strategies, including modification of the amplitude of kinematic parameters and positional error in addition to reduction of time to peak velocity and movement time. During stereotyped movements, most cerebellar thalamic neurones fired before movement onset and before VPLc neurones. During adaptation, this order of onset of firing was reversed, and cerebellar thalamic neurones discharged after VPLc neurones and close to the onset of movement. During motor adaptation, the mean rate of phasic ND rose in a large proportion of cerebellar thalamic and VPLc neurones, and the proportion of cerebellar thalamic neurones that encoded a signal about positional error and movement amplitude also increased. In addition, there is set-related activity in the discharge of a majority of cerebellar thalamic and VPLc neurones. This does not appear to be specifically related to motor adaptation, but is related to the movement amplitude. We have discussed the role of the cerebello-thalamo-cortical pathway in error detection in the light of the similarities between discharge patterns of cerebellar thalamic and VPLc neurones. We speculate that, when learned movements are performed, the discharge of cerebellar thalamic neurones occurs before movement, perhaps representing an efference copy of the intended movement. During adaptation, this signal is gated out, and later-arriving peripheral afferent input dominates cerebellar thalamic discharge.

Action Potentials↗
PubMed2006

Loudness adaptation in acoustic and electric hearing.

The present study is aimed to evaluate and compare loudness adaptation between normal hearing and cochlear-implant subjects. Loudness adaptation for 367-s pure tones was measured in five normal-hearing subjects at three frequencies (125, 1,000, and 8,000 Hz) and three levels (30, 60, and 90 dB SPL). In addition, loudness adaptation for 367-s pulse trains was measured in five Clarion cochlear-implant subjects at three stimulation rates (100, 991, and 4,296 Hz), three levels (10, 50, and 90% of the electric dynamic range), three stimulation positions (apical, middle and basal), and two stimulation modes (monopolar and bipolar). The method of successive magnitude estimation was used to quantify loudness adaptation. Similar to the previous results, we found that loudness adaptation in normal-hearing subjects increases with decreasing level and increasing frequency. However, we also found a small but significant loudness enhancement at 90 dB SPL in acoustic hearing. Despite large individual variability, we found that loudness adaptation in cochlear-implant subjects increases with decreasing levels, but is not significantly affected by the rate, place and mode of stimulation. A phenomenological model was proposed to predict loudness adaptation as a function of stimulus frequency and level in acoustic hearing. The present results were not fully compatible with either the restricted excitation hypothesis or the neural adaptation hypothesis. Loudness adaptation may have a central component that is dependent on the peripheral excitation pattern.

Acclimatization↗
PubMed1994

Non-reciprocal cross-adaptation of spiking responses of individual olfactory receptor neurons of spiny lobsters: evidence for two excitatory transduction pathways.

Single-unit spiking responses of 72 olfactory receptor neurons (ORNs) in the olfactory organ of the spiny lobster Panulirus argus were recorded extracellularly during presentation of a set of seven odorant stimuli (adenosine-5'-monophosphate, ammonium chloride, betaine, L-cysteine, L-glutamate, D,L-succinate and taurine) and analyzed in order to evaluate the response specificities of single ORNs and the independence of receptor sites. Individual ORNs often had narrow excitatory response spectra, but the most excitatory compound was different from neuron to neuron. These results suggest that these compounds can exert most of their excitatory effects through relatively independent receptor site types. To determine the relative independence of excitatory transduction processes in single ORNs for these stimuli, single-unit spiking responses of these neurons under conditions of self- and cross-adaptation were analyzed. The results demonstrate extensive cross-adaptation between pairs of the seven stimuli. When averaged across all neurons and all cross-adaptation conditions, cross-adaptation resulted in a mean reduction of 81% of the unadapted response. However, there were differences in the degree and pattern of adaptation for different pairs of compounds and for different neuron types (defined by most excitatory or 'best' chemical). For a given neuron type, there were significant levels of non-reciprocal cross-adaptation: neurons cross-adapted more when adapted to their best chemical than when adapted to their non-best chemicals. These results suggest the existence of two excitatory transduction pathways within an olfactory receptor neuron: one pathway activated exclusively by the best chemical and a second pathway activated by a broader spectrum of chemicals.

Acclimatization↗
PubMed1984

Changes in streptonigrin lethality during adaptation of Escherichia coli to picolinic acid. Correlation with intracellular picolinate and iron uptake.

Uptake studies with [14C]picolinate and 55Fe3+ have provided an explanation for the change in streptonigrin killing on adaptation of Escherichia coli to picolinate, in terms of the available iron within the cell. When picolinic acid is added to a growing culture of E. coli an interval of bacteriostasis ensues; this adaptation period is followed by resumption of exponential growth. Addition of picolinate (4 mM) to a log phase culture of strain W3110 gave protection from the lethal action of streptonigrin (30 microM) when the two agents were added simultaneously. In contrast streptonigrin killed cells that had adapted to picolinate; however, a preincubation of adapted W3110 with phenethyl alcohol protected the cells from streptonigrin lethality. [14C]Picolinate uptake studies showed that initially picolinate entered the cells, but that it was excluded from adapted cells; addition of phenethyl alcohol permitted the entry of picolinate into adapted W3110. The changes in streptonigrin killing parallel the changes in concentration of intracellular picolinate, which can chelate the iron required by streptonigrin for its bactericidal action. 55Fe3+ uptake studies showed that initially picolinate prevented iron accumulation by strain W3110, whereas adapted cells did take up iron in the presence of picolinate. Addition of phenethyl alcohol prevented any observed uptake of iron by adapted W3110. This modulation of iron transport by picolinate also affects streptonigrin lethality. Experiments with iron transport mutants showed that picolinate acted on both the enterochelin and citrate routes of uptake. Therefore picolinate affects the concentration of available iron within the cell both by (a) its intracellular presence resulting in chelation of iron and (b) its action on iron uptake; these effects explain the change in streptonigrin killing on adaptation of E. coli to picolinate.

Escherichia coli↗
PubMed2006

Risk-adaptive optimization: selective boosting of high-risk tumor subvolumes.

BACKGROUND AND PURPOSE: A tumor subvolume-based, risk-adaptive optimization strategy is presented. METHODS AND MATERIALS: Risk-adaptive optimization employs a biologic objective function instead of an objective function based on physical dose constraints. Using this biologic objective function, tumor control probability (TCP) is maximized for different tumor risk regions while at the same time minimizing normal tissue complication probability (NTCP) for organs at risk. The feasibility of risk-adaptive optimization was investigated for a variety of tumor subvolume geometries, risk-levels, and slopes of the TCP curve. Furthermore, the impact of a correlation parameter, delta, between TCP and NTCP on risk-adaptive optimization was investigated. RESULTS: Employing risk-adaptive optimization, it is possible in a prostate cancer model to increase the equivalent uniform dose (EUD) by up to 35.4 Gy in tumor subvolumes having the highest risk classification without increasing predicted normal tissue complications in organs at risk. For all tumor subvolume geometries investigated, we found that the EUD to high-risk tumor subvolumes could be increased significantly without increasing normal tissue complications above those expected from a treatment plan aiming for uniform dose coverage of the planning target volume. We furthermore found that the tumor subvolume with the highest risk classification had the largest influence on the design of the risk-adaptive dose distribution. The parameter delta had little effect on risk-adaptive optimization. However, the clinical parameters D(50) and gamma(50) that represent the risk classification of tumor subvolumes had the largest impact on risk-adaptive optimization. CONCLUSIONS: On the whole, risk-adaptive optimization yields heterogeneous dose distributions that match the risk level distribution of different subvolumes within the tumor volume.

Dose-Response Relationship, Radiation↗
PubMed2005

Use of adapted Aspergillus niger in the bioleaching of spent refinery processing catalyst.

Spent refinery processing catalyst is listed as a hazardous waste; the toxicity characteristic leaching procedure (TCLP) extracts of the catalyst are found to contain heavy metals at concentrations exceeding the regulated levels. In the present investigation, Aspergillus niger was adapted to single metal ions Ni, Mo or Al (at 100-2,000 mg/L in steps of 100mg/L) and then to a mixture of Ni, Mo and Al (at a mass ratio of 1:2:6, as approximately present in the spent catalyst). Adaptation experiments with single metals showed that the fungus could tolerate up to 1,000 mg/L Ni, 1,200 mg/L Mo and 2,000 mg/L Al. In the presence of a mixture of these metals, the fungus was able to tolerate up to 100mg/L Ni, 200mg/L Mo and 600 mg/L Al. One-step bioleaching experiments with 1 wt% spent catalyst (of particle size <37 microm) were carried out using un-adapted and various adapted fungal strains. In contrast to the adapted strains, the un-adapted strain showed no growth in the presence of the catalyst. Ni:Mo:Al-adapted strain was the most efficient in the leaching of metals from the catalyst (at 78.5% Ni, 82.3% Mo and 65.2% Al) over 30 days due to its tolerance to the toxic elements at 1 wt%. More importantly, the Ni:Mo:Al-adapted strain was capable of bioleaching up to 3 wt% spent catalyst. The TCLP extracts of the spent catalyst after bioleaching using the Ni:Mo:Al-adapted strain showed the concentrations of Ni and Mo were well within the regulated levels.

Aspergillus niger↗
PubMed2006

Adaptation to UVA radiation of E. coli growing in continuous culture.

Adaptive responses of bacteria to physical or chemical stresses in the laboratory or in the environment are of great interest. Here we investigated the ability of Escherichia coli growing in continuous culture to adapt to UVA radiation. It was shown that E. coli indeed expressed an adaptive response to UVA irradiation at an intensity of 50W/m(2). Cells grown in continuous culture with complex medium (diluted Luria Bertani broth) at dilution rates of 0.7h(-1), 0.5h(-1) and 0.3h(-1) were able to maintain growth under UVA irradiation after a transient reduction of specific growth rate and recovery. In contrast, slow-growing cells (D=0.05h(-1)) were unable to induce enough protection capacity to maintain growth under UVA irradiation. We propose that faster growing E. coli cells have a higher adaptive flexibility to UVA light-stress than slow-growing cells. Furthermore it was shown with flow cytometry and viability stains that at a dilution rate of 0.3h(-1) only a small fraction (1%) of the initial cell population survived UVA light-stress. Adapted cells were significantly larger (30%) than unstressed cells and had a lower growth yield. Furthermore, efflux pump activity was diminished in adapted cells. In a second irradiation period (after omitting UVA irradiation for 70h) adapted cells were able to trigger the adaptive response twice as fast. Additionally, this study shows that continuous cultivation with direct stress application allows reproducible investigation of the physiological and possibly also molecular mechanisms during adaptation of E. coli populations to UVA light.

Acclimatization↗