We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
Published online by Cambridge University Press: 22 January 2010
Introduction
Probably a very small biochemical change will give a host species a substantial degree of resistance to a highly adapted microorganism. This has an important evolutionary effect. It means that it is an advantage to the individual to possess a rare biochemical phenotype. For just because of its rarity it will be resistant to diseases which attack the majority of its fellows.
(Haldane 1949)As is clear from this passage, Haldane recognized that the temporary resistance conferred by rarity could lead to the maintenance of alleles involved in antagonistic coevolution. He then set out to explain the ‘surprising diversity revealed by serological tests,’ and suggested that some of the proteins uncovered in these tests ‘may play a part in disease resistance.’
Our purpose here is to review some of the more important theoretical and empirical advances since Haldane's time. We begin by considering simple genetic models of host-parasite interactions, with a particular interest in whether such interactions are expected to result in (1) stable equilibria for allele frequencies, (2) stable limit cycles of small amplitude, (3) stable limit cycles of large amplitude, or (4) unstable oscillations (see Fig. 1). We suggest that unstable oscillations, as well as stable oscillations having large amplitudes, can lead to the loss of genetic diversity, and discuss ways in which diversity could be protected, or at least re-supplied, if lost.
We then extend the discussion to consider the polygenic basis of resistance, and discuss the molecular evidence for the accrual of resistance genes in vertebrate genomes. It is clear that a profound revolution has taken place in our understanding of the genetic basis of disease resistance.
To save this book to your Kindle, first ensure [email protected] is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Find out more about the Kindle Personal Document Service.
To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.
To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.
