Biology Reference
In-Depth Information
Pathogens and parasites have very short generation times (hours to
days or weeks) compared with their hosts (months or years for honey
bees, depending on whether they are tropical or temperate). As a conse-
quence, pathogens and parasites evolve faster than their hosts and put
the hosts in the position of always evolving resistance (running), which
the pathogens and parasites are always evolving mechanisms to over-
come. h e model assumes that resistance in the host is based on a
single gene that is matched by a gene in the pathogen that lets it invade
and spread. Gene-for-gene resistance-interaction complexes have been
shown for plant-insect-pathogen systems. Polyandry and genetic re-
combination generate variation among the larvae in a nest. A pathogen
may get into a colony and into a larval host but not have the appropriate
genotype to develop well in that specii c larva. h e gene in the patho-
gen does not match the gene in the larva. But because the pathogen has
a very short generation time, it will not take long before a mutation or a
recombinant type occurs with a genotype that is very well suited to that
par tic u lar larval genotype. h e pathogen then increases in the larva,
and its of spring spread to the neighboring larvae. If the next larva it
spreads to has the same genotype as the original host larva, it will repro-
duce rapidly in that larva and spread to the next, and so on, eventually
weakening or killing all the larvae and the colony, as frequently hap-
pens with American foulbrood disease (Section 4.3.2). However, with
genetic recombination and polyandry, the probability increases that
the genotypes of the larvae nearby are dif erent from that of the current
larval hosts. When the pathogen spreads to a neighbor, it will not be
well adapted to it, the larva initially will have some degree of resistance,
and the spread of the disease will be slower. h e pathogen will need to
adapt to every new host it invades.
h e result is that genetic variation will be maintained in the popula-
tion for the genes engaged in the gene-for-gene arms race with the patho-
gen because there is no optimal or best genotype. h e same is true for
the pathogen: there is no optimal genotype. So this model satisi es the
criterion of a mechanism to maintain variation (presented in Section
4.2). Its action is the same as that presented for
csd
and the sex-
determination model. Selection is on the variance, not the mean ef ects.
