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Variation in Aggressiveness and the Regulation of Numbers in House Mouse Populations

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image of Netherlands Journal of Zoology
For more content, see Archives Néerlandaises de Zoologie (Vol 1-17) and Animal Biology (Vol 53 and onwards).

Three years of study were devoted to the search of a behavioural genetic mechanism for regulation of numbers in the house mouse (Mus. m.domesticus), following the lead of a pilot study suggesting applicability of the theory to this species. The hypothesis of a behavioural genetic mechanism, developed by Chitty and his school, maintains that (a) qualitative changes in behaviour are responsible for fluctuations in numbers of animal populations, and (b) these behavioural adjustments are underlain by shifts in frequency of genotypes. Chitty himself has always stressed the role of genotypes differing in aggressiveness: highly aggressive types having selective advantage under conditions of high density, and less aggressive (but more fertile) types being favoured in periods of low density. The first research problem posed by this hypothesis, is to investigate whether aggressiveness indeed has a genetic basis. Fortunately, in the house mouse a behavioural measure for aggressiveness (the Attack Latency) was available, for which a genetic component has been established by means of a selection experiment (VAN OORTMERSSEN & BAKKER, 1981). The emphasis of my work was to investigate the second premise of the hypothesis, that behaviour changes result from changes in density, as an outcome of shifts in genotype frequency. By establishing populations of feral house mice in small enclosures and following demographic changes in detail, conditions of high and low density were replicated several times. The aggressive level of the mice in these experimental populations was determined regularly by measuring Attack Latency (with the help of two methods: directly and testing offspring produced and raised in the laboratory), and periodically behaviour observations on the feral populations were done to detect correlations between various aggressive behaviours and demographic features. Attack Latency (AL) was measured on the border of familiar ground in a special testing procedure involving repeated tests of ten minutes each during which the subject was confronted with a subadult opponent of the same sex from an inbred albino stock. Tests were usually performed at the age of 14 weeks, and AL was expressed in seconds or as failure to attack. The measure proved applicable only to males, and cross-breeding experiments demonstrated a clear relation in AL-scores of fathers and their sons: the shorter the AL of a father, the shorter the AL of the sons, and the less often the sons failed to attack during the test procedure. Varying social experiences early on (presence or absence of father or litter mates, and being raised by the mother or a stepmother) did not result in measurable differences in AL. With increasing age, AL-scores tended to shorten and males failing to attack in the original tests started doing so. Nevertheless, the relative rank order according to AL remained the same in various groups of mice followed through the first six months of life. The stability of AL-ranking was noted regardless of whetherthe males had been isolated or had experienced several variants of group living in the meantime, provided however, that an isolation period of some weeks was intercalated before AL-testing. Having established the reliability and consistency of AL, it remained to demonstrate a clear relation between this measure and the occurrence of acts of overt aggression. Indeed a negative correlation was forthcoming: the shorter the AL, the more often did the individual perform aggressively (attacking, fighting and chasing). The next phase of the study involved setting up experimental populations to allow repeated observation of demographic change associated with fluctuations in numbers. The mice were housed in small barns ("mouse houses") equipped with transparent tube structures. Food, water and nesting materials were always present in excess, and the mice were protected from predators. Every week the nestling contingent was monitored, and every four weeks an extensive census was undertaken during which all mice were handled, and mice weaned since the previous census received an individual code on the basis of toe-clipping. Behavioural observations were concentrated in the first half of 1977, when in all populations numbers rose to peak densities. Emigration in the configuration of the experimental populations implied an artificial way of removing mice. Although not offering the same options open to dispersal in a natural situation, under a wide variety of experimental conditions, the degree of definitive emigration was not affected. In some experiments movement of mice between the various mouse houses was allowed, and livetrapping revealed that the mice living in one house constituted a reproductive unit comparable in all respects with the deme known from field-work. Since the unit of study was the mouse house and its inhabitants, my work can be seen as a test of the Chitty Hypothesis at the level of the deme. Ten replicas were followed in the period 1976-1978, involving a maximum of four fluctuations. The experimental populations included replicas from wild stock caught locally as well as replicas with mice from the selection line for Short Attack Latency (SAL) of VAN OORTMERSSEN & BAKKER (1981). If selection for aggressive genotypes plays as dominant a role as the theory demands in the regulation of numbers, then obvious differences in level and timing of peak densities would be expected between these two types of replicas. In fact, the course of numbers and sequence of change in demographic parameters proved to be nearly identical in both. In order to monitor the AL-score distribution in a deme, male mice were removed and transported to the laboratory where alternative techniques were used to determine the "AL-profile". Originally only adults were transferred, and their AL was determined on the basis of male offspring produced and raised in the laboratory, designed to provide an indication of the inherent AL-level of the males. Equally reliable and much less time-consuming proved to be the direct AL-determination of the males taken from the deme: adults were tested after an isolation period of some weeks, and nestlings at 14 weeks after being raised in a standard fashion. Following the various procedures an adequate sampling of the male population was assured, thus providing a profile of AL-values as an indication of aggressive level for each deme. The AL-profiles obtained failed to reveal changes in genetic composition with time, and the difference initially present between selected (SAL) and wild-type demes was maintained throughout. AL-profiles of territory holders were indistinguishable from those of emigrants, and both did not differ from the profiles of transplanted nestlings. To elucidate this problem, a further series of experiments examined the relation between AL-scores and the probability of territory establishment respectively winning contests in a border situation. Any effect of inherent aggressiveness as measured by AL was apparently overruled in these situations byThe most striking feature of the work in the mouse houses was the discovery of a density-dependent behavioural regulation mechanism. Nestling mortality was the prime numerical adjustor, and was found to depend on maternal disturbance, itself primarily triggered by the number of agonistic interactions of territorial males. Both during an increase as well as an ensueing decrease, a threshold value in the size of the male contingent old enough to be involved in territorial behaviour (older than 8 weeks) was apparent: in the context of the mouse houses used in this study fixed at approximately 20 individuals, above which limit nestling mortality rose sharply to reach 100%. Repression of sexual maturation in females was also observed under conditions of high density. Thus a behavioural regulation mechanism appears to be sufficient to account for the causation of fluctuations in numbers in house mouse demes, without the need to invoke underlying shifts in genetic composition concerning aggressiveness, at least as far as this is reflected in AL.

Affiliations: 1: Institute of Genetics and Zoological Laboratory, University of Groningen, The Netherlands


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