When culture changes much more rapidly than the genome can respond, “mismatch” diseases occur.

The immune system is based on molecular recognition of commensal and pathogenic microbes.22

Global spread of humans out of Africa over the last 70 000 years resulted in variations in genome–based disease resistance as new environments and pathogens were encountered.17

For evolutionary medicine, the causes of disease are more simply conceived.3

Another very likely factor, however, was the remote location of this population.

These genomes were then compared to the genomes of individuals who lived in both the lowland and highland areas during prehistoric and modern times,

researchers would like to find DNA older than 11,000 years

“Looking at the bumps and shapes of a head does not help you understand the true genetic ancestry of a population—we have proved that you can have people who look very different but are closely related.”

, quashing a longstanding theory that a group of Paleoamericans existed in North America prior to Native Americans.

By sequencing and analyzing 15 ancient genomes found throughout the Americas—six of which were older than 10,000 years

which an allelethat confers resistance to human diseases (suchas tuberculosis or leprosy

Gene flow of multiplerodent species (44,65) and at least one marsupial(66) is facilitated by corridors of natural vegeta-tion within cities.

and subsequently diverged into aseparate form (C. pipiensf. molestus), which isreproductively isolated from and less geneticallydiverse than surface populations (52).

Redfoxes (Vulpes vulpes) recently colonized Zurich,Switzerland, which resulted in lower genetic di-versity in city foxes compared with that in nearbyrural populations (50)

Urbanization is predicted to strongly influencegenetic drift, which produces stochastic changesin allele frequencies between generations.

Many other changesin morphology, behavior, physiology, and geneexpression have been reported in urban popula-tions (26), but the genetic basis of these changeshas often not been established and may often beexplained by phenotypic plasticity, which is aninterestingphenomenoninitsownrightbutbe-yond the scope of this article (14,27).

In this Review, we ask whether urbanizationaffects evolution through a comprehensive reviewof the evidence for evolutionary change in urbanenvironments and the mechanisms that causethese changes.

pplied evolutionary studies couldlead to more effective mitigation of pests anddisease agents.

how often do native and exotic speciesadapt to the particular environmental challengesfound in cities?

The first, a loss of “ardour” by the males, is not a very satisfying explanation in the context of our modern understanding of sexual selection.

Because the ornament is condition dependent, it is always a reliable indicator of genetic quality,

. However, under some circumstances, this model results in a self-reinforcing, open-ended process that produces never-ending trait elaboration. Eventually, the process is opposed by natural selection when the ornament becomes so large as to be a major impediment to survival, a point that was actually well appreciated by Darwin (1871).

The higher-quality females are ready to breed before the lower-quality females, and they choose to pair with the higher-quality males (Fig. 9.1C).

Thus, the difficulty, which partly remains unsolved, is to understand the evolution of female (or male) preferences.

Darwin’s approach was to contend that it was inconceivable that preferences did not exist and to provide evidence of female preferences in various animal species.

In some species, males engage in fierce struggles among one another, and the victors in these contests tend to mate with the receptive females.

Thesestudiesillustratethepotentialinfluenceofenvironmentalvari-abilityontestosteronelevels,andtheorysuggeststhatenvironmentalfactorscanalterthereliabilityofsexualsignals,promotingorpreventingtheirevolution(see[58,61,62]).

Nevertheless,thepositivelinksbetweenthelevelofsignalexpressionandlongevityorfecundityhasnotdefinitivelybeenestablished,butmostlyinferredfromotherindicatorsofhealthstatus(reviewedin[24,29,30])or,inthecaseoflongevity,deducedfromoverwintersurvivalratesinavianspecies[31–36].

Recently,theoxidativestressconcepthasgainedempiricalsupport,andis consideredaubiquitousselectivepressureabletoshapeindividualphenotypesfromconceptiontodeath[14,15].Thus,it hasbeenhypothesizedthatoxidativestresscouldbeanimportantcostofreproductioninfluencingfecundityvs.survivaltrade-off[16–19].Thatcostcouldnotonlybetheconsequenceofincreasingcellmetabolismduringreproduction(butsee[19])butalsoduetoresourceinvestmentsinsexualsignals(e.g.[20])thatwouldthenfavormatingandrepro-ductivesuccess[15].Amongpotentialsignalsinvolvedintheoxidativecostofreproduction,coloredornamentsgeneratedbycarotenoids(manyyellow-to-redtraits)areprobablythebestknowninvertebrates(e.g.[20–22]).

Such efforts will also include observationaldata provided by the broader public [71].

One particularly exciting avenue ofresearch afforded by new genomic tech-nology is the possibility of directly observ-ing the dynamics of evolution

Models of mutation, inheritance, andselection have inspired the development ofcomputational evolutionary algorithmsthat are used to solve complex problemsin many fields [53,54].

ion of speciesand ecosystems [13,39–42]. Linking spa-tial data on phenotypes, genomes andenvironments in a phylogenetic contextallows us to identify and name Earth’sdiverse life forms. This linkage, in turn,helps to provide the basic units needed toquantify taxonomic diversity and to pursueits conservation.

Unfortunately, geneticallymodified crops are genetically uniformand so do not represent a long-termsolution against the evolution of eitherherbicide or Bt resistance.