Copyright 0 1990 bv the Genetics Societyof America
Alan Robertson
ALANROBERTSON was born on February 2 1, 1920,
in Preston, England, and died in Edinburgh on April
25, 1989, after a longillness. His early education was
at the Liverpool Institute, and he then went on to
Gonville and Caius College, Cambridge University,
from which he graduated with a B.A. in Chemistry in
194 1. He commenced postgraduate research in phys-
ical chemistry at Cambridge but his studies were in-
terrupted by the outbreak of World War 11; he pub-
lished several papers on physical chemistry but did
notcomplete his Ph.D. ALANworked with C. H.
WADDINGTONOperational
in Research during thewar
and subsequently was invited to joinWADDINGTON in
the Agricultural Research Council Animal Breeding
and Genetics Research Organization (ABGRO), ini-
tially at Hendon and later in Edinburgh. He studied
with SEWALL WRIGHTin Chicago and JAY LUSH in
Ames in 1947, then returned to ABGRO in Edin-
burgh. He remained in Edinburgh for the rest of his
career in what became the ARC Unit of Animal
Genetics, directed initially by WADDINGTON and later
by DOUGLAS FALCONER, and was promoted to Deputy
Chief Scientific Officer in 1966. ALANreceived a
D.Sc. from the University of Edinburgh in 1951 for
his work in genetics and was appointed an Honorary
Professor in 1967. He was appointed OBE (Order of
the British Empire) in 1965 and received many other
honors for his contributions to science, notably elec-
tion as a Fellow of the Royal Society of London in
Generics 125: 1-7 (Mav. 1990)
(1920-1989)
1964 and of Edinburgh in 1966, a Foreign Associate
of the National Academy of Sciences of the USA in
1979, a Foreign Honorary Member of the Genetics
Society of Japan, and a Member of the Spanish Real
Academia de Ciencias Veterinarias. He was also
awarded honorary doctorates from the University of
Stuttgart-Hohenheim, the Agricultural University of
Norway, the State University of Liiige and the Danish
Agricultural University. ALANis survived by his wife
MEG, whom he married in 1947; his three children,
MARK, HILARY andMICHAEL;and three grandchil-
dren.
ALANROBERTSON'S early contributions to genetics
were in the field of animal breeding and primarily
focused on breeding dairy cattle for increased milk
production (although one of his first papers, with M.
LERNER, was an analysis of the heritability of a thresh-
old trait, viability, in poultry). In the mid-1940s to
1950s animal breeding theory was in its infancy. To-
gether with J. M. RENDEL, and prompted by the ideas
of LUSH(1947) and DICKERSON and HAZEL(1944),
ROBERTSON showed how the genetic gain per year
resulting from mass selection for milk yield depended
on the relative selection differentials and generation
intervals in the four pathways for breeding replace-
ment bulls and cows each generation: cows to breed
bulls, cows to breed cows, bulls to breed bulls, and
bulls to breed cows. RENDELand ROBERTSON (1950)
showed that, with no progeny testingof bulls, progress
2 T. F. C. Mackay
depended on selecting cows on their own perform-
ance, and that the maximum rate of progress that
could be expected was an increase of 1% of the
average yield per year in a small herd. ROBERTSON
and RENDEL(1950)demonstratedthat,although
progeny testing ofbulls resulted inonly a modest
increase in genetic gain to 1.1% per year in a small
herd (because the increase in generation interval nec-
essary to evaluate the bull’s breeding value offsets the
gain in selection differential), with artificial insemi-
nation the herd size could be increased 20-fold, so
that progeny testing of bulls together with perform-
ance testing of cows could give a theoretical rate of
progress of 1.7% per year.
Having demonstrated quantitatively the theoretical
merits of progeny testing,ALANROBERTSON set about
considering the practical problems of implementing a
progeny testing scheme on a national level. In a breed-
ing program using progeny testing,most selection can
be placed on the “bull to breed bull” pathway. ROB-
ERTSON showed with A. A. ASKER(195 1) thatselection
decisions made in a few herds greatly dominate the
genetic improvement of the breed as a whole. Herds
of British Friesian cattle (and of eight other breeds;
ROBERTSON1953) can be grouped into three tiers.
The top tier, composed of a few herds, breeds supe-
rior bulls, which are sold or used by multiplier herds
in the second tier; sons of these bulls are then sold to
the third groupcomprising the bulk of the herds. The
problem then reduces to one of finding methods to
evaluate bullsin the top tier and using them most
efficiently to breed future sires. Progeny testing, of
course, involves estimating bulls’ breeding values on
the basis of theperformance (milk yield) of their
daughters. If the daughtersof the various bulls under
test are unevenly distributed among herds, variation
in management practices leading to different produc-
tion levels between herds and between years will se-
riously confound the estimation of the bulls’ breeding
values. This led ROBERTSON and RENDEL(1954) to
suggest the“contemporarycomparison”method of
evaluating bulls, whereby the average yield of a bull’s
daughters in a given herd andyear is compared to the
average yieldof other cowsin that herd and year,
taking into account the number of animals in each
group. The tested bulls can then be ranked and the
best chosen to breed young sires. This method works
best if the rank order of breeding values is the same
regardless of the overall level of production of the
differentherds,and if the accuracy in estimating
breeding values does not differ for different produc-
tion levels (that is, if there is no genotype by environ-
mentinteraction between milkyield and plane of
nutrition). The absence of such genotype by environ-
ment interaction was shown to be true generally (MA-
SON and ROBERTSON 1956), and in 1954 the contem-
porary comparison method of progeny test evaluation
was adopted by the Milk Marketing Board of England
and Wales. It has been used extensively in the dairy
cattle industry in Great Britain, and only recently has
theadvent of schemes formultiple ovulation and
embryotransfer(MOET)promisedtochangethe
basic structure of the industry-as had been foreseen
by RENDELand ROBERTSON (1950) as a method for
increasing the contribution to genetic gain from the
“COW to breed cow” pathway.
ALANROBERTSON was concerned with the family
structure of the breeding population for three rea-
sons. First, it is important for optimizing progress per
year because of the conflict between testing few bulls
with manydaughters, thus obtaining reliable estimates
of breedingvalue, or many bulls withfewer daughters,
thus giving greater selection differential. ROBERTSON
(195’7) showed quantitatively how best this balance
might be achieved. Second, the efficiency of a breed-
ing program depends on the accuracy of the estimates
of the heritablilities and genetic correlations of the
selected traits. Suchestimates are notoriously variable,
and ROBERTSON(1959a,b; 1962) and LATTER and
ROBERTSON (1960) showed how the accuracy could
be improved with the use of efficient experimental
design. Third, selection causes inbreeding both be-
cause the selected parents area restrictedsample from
the population and because selection increases the
proportion of genes in common in the selected group
(ROBERTSON 196l), leading to inbreeding depression
and loss of genetic variation in selection lines.
The mid-1950s marked the beginning of the flood
of information that was to become available on bio-
chemical polymorphisms in populations, and animal
breeders were quick to question what use this infor-
mation might bein improving productionin domestic
livestock. There was initial excitement about associa-
tions between blood group polymorphisms and traits
of commercial importance in dairy cattle and poultry
as an aid to selection, but ALANROBERTSON raised the
following important caveats to searching for associa-
tions between marker loci and quantitative trait loci
(QTLs) that remain equally relevant today (NEIMANN-
SBRENSEN and ROBERTSON 1961). (1) If the association
is caused by linkage, there will notbean overall
association between the markers and QTLs in a pop-
ulation at linkage equilibrium, although a transient
association may occur following a cross of two popu-
lations or if the marker locus and Q T L are closely
linked. (2) Statistical problems arise because multiple
simultaneous tests of association are made between
the marker loci and production traits, causing spu-
rious false positive associations if care is not taken to
set the overall significance level to compensate for the
number of tests and to remove sets of quantitative
traits that are highly correlated genetically. Even so,
 Alan Robertson ( 1 920-1 989)
different associations may prove significant in differ-
ent samples. (3) Real associations between marker loci
and QTLsmay be different in different genetic back-
grounds, so that the same correlations will not neces-
sarily be found in different populations. (4) The prac-
tical value of taking accountof an association between
a marker locus and a QTL in selecting animals de-
pends on whether the proportion of the genetic vari-
ance of the traitexplained by the association ap-
proaches the heritability of the trait. The proportion
of genetic variance attributable to significant blood
group associations is generally very small.
These problems, coupled with his growing convic-
tion that the number of loci responsible for most of
the variation for quantitative traits is small compared
to the potentially large number of biochemical poly-
morphisms, led ALANto doubt theutility of searching
for associations between the two categories of traits.
By 1966 he was convinced that the future of animal
breeding wasin understanding the biochemical and
physiological correlates of response to selection. Sev-
eral research projects measuring such correlates of
response to selection for growth rate in mice were
laterinitiated by his colleagues in Edinburgh (e.g.,
BRIENet al. 1984; SHARPet el. 1984).
ALAN ROBERTSON recognized from the beginning
the greatvalue of molecular polymorphisms in tracing
the history of populations, and thought the most in-
teresting question to be addressed waswhy so much
variation was maintained at theseloci.Finding no
evidence that heterozygotes forblood group loci were
superior to homozygotes with regard to production
characteristics in dairy cattle, he suggested that such
polymorphisms were neutral (NEIMANN-SORENSEN
and ROBERTSON 1961) before the formalproposal of
the neutral mutation, random drift theory of molec-
ular evolution (KIMURA1968). ALANretained his in-
terest in the growing field of molecular evolution,
following the unfolding globin gene-family story with
particular interest, and was often asked to speak to
animal breeders on the application of molecular biol-
ogy to animal improvement.
Dairy cows are not themost tractable of experimen-
tal animals, and early in his career ALANROBERTSON
turned his attention to Drosophila melanogaster as a
model system with which to examine the validity of
existing theory, to determine in what way the theory
neededtobeextended to cope with discrepancies
between observed and predicted results, and to inves-
tigatethe nature of quantitativegenetic variation.
This interaction between experimental and theoreti-
cal research can be traced from the now classic series
of papers on an experimental check of quantitative
genetic theory with his colleagues G . A. CLAYTON, J.
A . MORRISand G . R. KNIGHT. Selecting for increased
and decreased numbers of abdominal bristles from a
3
randomlybredpopulation, CLAYTON,MORRISand
ROBERTSON (1957) showed that the short-term aver-
age response of replicate populations agreed well with
that predicted from estimates of heritability in the
base population, and thatgenes controlling abdominal
bristle numberact additively and are neutral with
respect to fitness. However, the long-term response
was unpredictable (CLAYTONand ROBERTSON 1957),
often reaching a plateau at which genetic variability
was still present due to the maintenance of homozy-
gous lethal or sterile genes with heterozygous effects
on bristle number, so that artificial selection was bal-
anced by natural selection. In lines selected for low
bristle number, a sudden rapid response in females
was accompanied by an increase in variance; this was
later inferred to be caused by mutations at the bobbed
locus (FRANKHAM 1980). Correlated response of ster-
nopleural bristle number could not be well predicted
from the correlations in the base population (CLAY-
TON et a l . 1957). The primary questions to emerge
from these experiments were how to predict limits to
selection for given population sizes and selection in-
tensities, what determines the response of a character
not directly selected in a line selected for another
trait, and what are the relationships among quantita-
tive traits and fitness and its components. ALANROB-
ERTSON and his colleagues addressed these problems
theoretically and by further experimentation.
Fora simple additivemodel, ROBERTSON(1960)
showed that the expectedlimit to artificial selection is
equal to the expected response in the first generation
multiplied by twice the effective population size, with
a half-life of 1.4 times the effective population size.
The theoretical limit is the same if two populations of
size N are selected independently and then crossed
and reselected, or if a single population of size 2N is
selected. These predictions were found to hold gen-
erally true for experimentalpopulations (JONES,
FRANKHAM and BARKER1968; MADALENA and ROB-
ERTSON 1975). The theory of limits to artificial selec-
tion was later extended to include the effects of link-
age (HILLand ROBERTSON1966; ROBERTSON1970,
1977). The effect of linkage on thefinal limit depends
on population size, the problem being whether the
negative associations between linked loci withopposite
effects on the trait caused by selection can be broken
by recombination before they are fixed by chance.
The general consensus is that linkage will not substan-
tially reduce the limit to selection expected with free
recombination for most combinations of parameters
relevant to selected populations. This was confirmed
experimentally by MCPHEEand ROBERTSON (1970).
Drosophila selection lines, in whichrecombination was
suppressed over 80% of the genome, reached limits
to selection for sternopleuralbristle number that were
reduced 25% from limits achieved with free recom-
4 T. F. C. Mackay
bination. NICHOLASand ROBERTSON (1980) further
extended the theory of limits to artificial selection to
the case where thelimit is caused by a balance between
natural and artificial selection, showing a reduction in
the final limit and maintenance of genetic variation at
the limit, as observed experimentally. Natural selec-
tion must be very strong before this sort of plateau is
achieved.
The problem of unpredictable correlated responses
to selection raised by the early Drosophila experi-
ments was investigated using computer simulation by
BOHREN,HILLand ROBERTSON(1966). The asym-
metrical correlated responses to selection often ob-
served in practice couldbeexplained because the
genetic covariance between two characters is very
sensitive to changes in gene frequency caused by se-
lection or drift, so that the predictive value of the
genetic covariance estimated in the base populations
does not hold for many generations.
ALANROBERTSON saw selection experiments with
laboratory animals as most useful in determining the
nature of quantitative genetic variation in terms of
the forces creating and maintaining variation for
quantitativetraits, andthenumbers, effects, gene
frequencies and interactions of loci controlling them.
The extent to which spontaneous and X-ray-induced
mutation causes genetic variation for bristle traits was
examined by CLAYTON and ROBERTSON (1955, 1964)
by response to selection of populations of different
genetic origin (highly inbred, plateaued, and geneti-
cally variable base populations). The concept of mu-
tational variance (the input of new additive genetic
variance pergeneration) was introduced,and was
estimated from thevarious experiments to be roughly
times the environmental variance (VJ for spon-
taneousmutations and 0.003 V, for X-ray-induced
mutations. CLAYTON and ROBERTSON (1955) empha-
sized that this mutation rate was large in an evolution-
ary context, and that levels of variation observed in
natural populations could easily be obtained by mu-
tation-drift balance for a neutral character in a small
population. Genes of large effect oftenappear in
selection lines, for example recessive lethal chromo-
somes (e.g., CLAYTON and ROBERTSON 1957) or visible
recessive genes (e.g., MADELENAand ROBERTSON
1975) with heterozygous effects in the direction of
selection. With a view to distinguishing whether these
genes of large effect were initially present in the base
population or had arisen de novo during selection by
mutation or recombination, ROBERTSON and NARAIN
(1 97 1) determined theoretically the average age and
average time to elimination of recessive lethals in small
populations, and ROBERTSON (1978) derived the dis-
tribution of time before a single copy of a recessive
gene appears as a homozygote in a later generation.
ROBERTSON (1 955) proposed that the maintenance
of genetic variation for quantitative traits could be
understood in terms of their relationships with fitness,
and thatquantitative traits could be divided into three
broad categories: traitsperipheralto fitness, traits
with an intermediate optimum, and major fitness com-
ponents. For the first category, neutral traits, varia-
tion in thetrait is not associated with variation in
fitness, populations harbor a large amount of mostly
additivegeneticvariation, there is no inbreeding
depression, and variation islikely maintained by a
balance of mutation and drift. At the other extreme
are major componentsof fitness for which populations
display small amounts of mostly nonadditive genetic
variation, possibly maintained by a balance between
mutation and selection against deleterious recessives
at mostloci and overdominance at some loci. Such
traits characteristically exhibit severe
inbreeding
depression, and are expected to be negatively geneti-
cally correlated with other major components of fit-
ness. ALANROBERTSON was intrigued by the fact that
the population means of quantitative traits were sta-
ble. He evaluated the hypothesis that this stability was
a consequence of an intermediate optimum with re-
spect to fitness. Individuals with extreme values of the
traits are more fit either because stabilizing selection
acts directly on the trait or because extreme individ-
uals are more homozygous and heterozygotes are less
fit. For both models there are problems explaining
the maintenance of variation for these traits.ROBERT-
SON (1956) showed that stabilizing selection leads to
fixation at loci affecting the selected trait and de-
creases genetic variation for the trait. ALAN was in
any case not happy with the stabilizing selection model
because of its implicit assumption that selection acts
on genes only through their effects on a single char-
acter, which is perhaps why hedidnotconsidera
balance between mutation and stabilizing selection as
a model for maintaining variation. However, neither
can heterozygote advantage be generally true, because
of the genetic load incurred.
Having conceived the above theoretical framework,
ROBERTSON then proposed several experiments to test
the strengthof natural selection acting on quantitative
traits, many of which he and his colleagues applied to
Drosophila bristle number. One test of the strength
of stabilizing natural selection is to perturb thepopu-
lation mean of a trait by a few generations of artificial
selection, then relax artificial selection (to determine
if stabilizing natural selection will change the mean
toward its initial value) and apply artificial selection
in the opposite direction (to determine the amountof
remaining genetic variation for the trait).If the mean
of the trait does not alter under relaxed selection but
responds to reverse selection, then strong stabilizing
selection does not operate on the trait. Several pub-
lished (CLAYTON, MORRISand ROBERTSON 1957) and
 (1920-1989) Robertson Alan
unpublished experiments of this sort were conducted
in ROBERTSON’S laboratory to determine the strength
of stabilizing selection for Drosophila bristle traits. In
all cases the means of the selected lines responded
little to relaxed selection, despite considerable resid-
ual genetic variation at the time selection was sus-
pended. Another approach is to manipulate chromo-
somes from lines selected forhigh and low bristle
score so that one chromosome is heterozygousfor
chromosomes from the high and low selection lines,
and the others arehomozygous for either the low or
high bristle background. Because the optimum model
involves fitness interactions between loci, if stabilizing
natural selection acts on the trait, the mean bristle
score will increase when the segregating chromosomes
are in a low background and decrease when they are
in a high background. ALAN ROBERTSON personally
performed several several such experimentsand
found no tendency forthe mean scores of his synthetic
populations to change (ROBERTSON 1967). These ob-
servations led ROBERTSONto conclude that, at the
majority of loci controlling variation for bristle traits,
the segregating alleles are neutral with respect to
fitness. LATTERand ROBERTSON (1962) directly meas-
ured the fitness of lines selected for several genera-
tions for two bristle characters and wing length, using
a methodof fitness estimation devised by KNIGHTand
ROBERTSON (1957). After five generations of selec-
tion, the mean fitness of abdominal bristle lines de-
clined 28% relative to unselected controls, and the
wing length lines by 7%, with evidence of low lines in
all cases being less fit than high selection lines. This
was again interpreted to argueagainst strong stabiliz-
ing selection for those traits in the base population.
ALAN’Sfinal Drosophila experiment was also con-
cerned with this question. He proposed to measure
directly relative fitness of homozygous chromosomes
with different bristle numbers by competition with a
marked balancer, and to determine whether fitness
changes on changing the genetic background.
The description of quantitative variation in terms
of the gene frequencies, numbers,and effects and the
interactions of the individual loci controlling the traits
is necessary if quantitative genetics is to evolve beyond
statistical descriptions. ALANROBERTSON spoke often
of these problems inhis reviews (e.g., ROBERTSON
1967, 1968) andwas actively involved in experiments
to address these questions. The theory of limits to
artificial selection (ROBERTSON 1960) in fact suggests
an experimental approach to inferring gene frequen-
cies at loci involved in selection response. I f the initial
population size is restricted by inbreeding, the limit
to selection from the bottlenecked lines will be re-
duced over that obtained fromselection from a large
base population by an amount that depends on how
important are initially rare genes (eliminated from the
5
bottlenecked lines) in determining selection limits. J.
M. P. DA SILVA(1961), a Ph.D. student of ALAN’S,
showed that selection from a single pair resulted in a
reduction of the limitby 30%, suggesting that the
majority of alleles fixed by selection were not initially
rare.
The ultimate goal is to identify the individual loci
responsible for quantitative variation, and in this con-
text ALAN ROBERTSON was encouraged by the work
of THODAY and his colleagues (reviewed in THODAY
1979) in mappingQTLs. ROBERTSON was quick to
point out that the question being addressed by these
studies was not how many loci affect the variation for
a quantitative traitbut, rather,how many loci account
for the bulk of the difference between selected lines
(e.g., ROBERTSON 1967, 1968). ALANviewed the dis-
tribution of gene effects on quantitative traitsas being
such that most loci have small effects, but a few have
large effects and cause mostof the variation. MC-
MILLANand ROBERTSON (1974) showed that the re-
sults of Q T L mapping experiments using recombina-
tion of an extreme-scoring chromosome with a mul-
tiply marked tester chromosome to identify regions
with significant effects on the trait will always over-
estimate the effect of detected loci and underestimate
their number (because several linked loci affecting the
trait may occur in a segment) and can even identify
loci that donot exist if the assumption that all loci on
the tested chromosomes carry “higher” alleles than
loci on the tester chromosome is violated. A practical
suggestion for partially alleviating the latter problem
is to ensure that tester and tested chromosomes are
selected in opposite directions from the same base
population, with subsequent backcrossing of the
markergenesintothetesterchromosome. Such a
third chromosome was synthesized in ALANROBERT-
SON’S laboratory and used by his Ph.D. students L. R.
PIPERand A. E. SHRIMPTON to partition the effect of
a high sternopleural bristle number chromosome into
segments bounded by recessive visible markers. The
results (SHRIMPTON and ROBERTSON1988a, b) sup-
port themodel of distribution of gene effects outlined
above despite the methodological problems.
This review of ALAN ROBERTSON’S work isin no
sense comprehensive but I hope, forthose not familiar
with this subject, that it has conveyed a sense of the
breadth of his contribution to quantitative genetics
from its most practical application in animal breeding,
through statistical methodology, theoretical underpin-
nings and tests of the theory, evolutionary implica-
tions and, finally, to the Mendelian genetics of quan-
titativetrait loci. For those who actively workin
quantitativegenetics,perhaps it will serve as are-
minder that muchof the accepted folklorein this field
can be traced back to ideas of ALANROBERTSON, and
areas in which these have been extended subsequently
6 T. F. C . Mackay

and formalized by others will be recognized.[For HILL, W. G., and T . F. C. MACKAY, 1989 EvolutionandAnimal
more comprehensive reviews of the contributions of Breeding. C.A.B. International, Wallingford.
HILL,W. G., and A. ROBERTSON, 1 9 6 6 T h e effects of linkage on
ALANROBERTSON, see HILL and MACKAY(1989).] limits to artificial selection. Genet. Res. 8: 269-294.
Although his scientific publications reveal an astonish- JONES,L. P., R. FRANKHAM andS .J.F. BARKER, 1968 Theeffects
ing range of interests, ALAN’S influence through per- of population size and selectionintensity in selection for a
sonal contact was undoubtedly his most lasting contri- quantitative character inDrosophila. 11. Long-term response to
bution. For those who studied atthe Institute of selection. Genet. Res. 12: 249-266.
KIMURA,M., 1968 Evolutionary rate at the molecular level. Na-
Animal Genetics in Edinburgh, ALAN’S daily informal ture 217: 624-626.
coffee sessions were an invaluable opportunity to ex- KNIGHT,G. R., and A. ROBERTSON, 1957 Fitness as a measurable
change ideas and meet other workers in the field who character in Drosophila. Genetics 42: 524-530.
were attracted to Edinburghby the presence of ALAN LATTER,B. D. H., and A . ROBERTSON, 1960 Experimental design
and his colleagues. ALANwas invariably generous with in the estimation of heritability by regression methods. Bio-
metrics 16: 348-353.
his time and ideas, and could always be approached LATTER, B. D. H.,andA. ROBERTSON,1962 T h e effectsof
for advice by studentsand colleagues alike. Many inbreeding and artificial selection on reproductive fitness. Ge-
scientists currently working on quantitative genetics net. Res. 3: 110-138.
can trace their roots either directly or indirectly to LUSH,J. L., 1947 Family merit and individual merit as bases for
ALANROBERTSON at the Institute of Animal Genetics selection. Am. Nat. 81: 241-261; 362-379.
MADALENA, F. E., and A. ROBERTSON,1975 Population structure
of the University of Edinburgh; more than anything in artificial selection: studies with Drosophila melanogaster. Ge-
this must be a tribute tohis influence. net. Res. 24: 113-126.
MASON,I . L., and A. ROBERTSON,1956 The progeny testing of
I wish to thank M. ROBERTSON, W. G. HILL, R. C.ROBERTSand dairy bulls at different levels of production. J. Agric. Sci. 47:
B. S. WEIR for comments on the manuscript. This work was sup- 367-375.
ported by National Institutes of Health Quantitative Genetics Pro- MCMILLAN, I . , and A. ROBERTSON, 1 9 7 4 T h e power of methods
gram grant GMI 1546 and a NATO award for collaborative re- for the detection of major genes affecting quantitative charac-
search. This is Paper No. 12532 of the Journal Series of the North ters. Heredity 32: 349-356.
Carolina Agricultural Research Service. MCPHEE, C. P., and A. ROBERTSON, 1970 T h e effect of suppress-
ingcrossing-over on the response to selection in Drosophila
TRUDY F. C. MACKAY melanogaster. Genet. Res. 16: 1-16.
Department of Genetics NEIMANN-SBRENSEN, A , , and A . ROBERTSON, 1961 T h e association
North Carolina State University between blood groups and several production characteristics
in three Danish cattle breeds. Acta Agric. Scand. 11: 163-196.
Raleigh, North Carolina 27695-7614 NICHOLAS, F. W., and A. ROBERTSON, 1980 The conflict between
naturalandartificialselection in finitepopulations. Theor.
LITERATURE CITED Appl. Genet. 5 6 57-64.
RENDEL, J. M.,and A. ROBERTSON,1950 Estimationofgenetic
BOHREN,B. B., W. G. HILLandA. ROBERTSON,1966Some gain in milk yield by selection in a closed herd of dairy cattle.
observations on asymmetrical correlated responses to selection. J. Genet. 50: 1-8.
Genet. Res. 7: 44-57. ROBERTSON, A,, 1953 A numerical description of breed structure.
BRIEN, F. D.,G.L. SHARP, W. G. HILLand A. ROBERTSON, J. Agric. Sci. 43: 334-336.
1984 Effects of selection on growth, body composition, and ROBERTSON, A,, 1955 Selection in animals: synthesis. Cold Spring
food intake in mice. 11. Correlated responses in reproduction. Harbor Symp. Quant. Biol. 20: 225-229.
Genet. Res. 44: 73-85. ROBERTSON,A,,1956Theeffectof selectionagainst extreme
CLAYTON,G.A,, J. A. MORRISand A. ROBERTSON,1957An deviants based on deviation or on homozygosis. J. Genet. 54:
experimental check on quantitative genetical theory. I. Short- 236-248.
term responses to selection. J. Genet. 55: 131-151. ROBERTSON, A,, 1957 Optimum group size in progeny testing and
CLAYTON, G. A,, and A. ROBERTSON, 1955 Mutation and quanti- family selection. Biometrics 13: 442-450.
tative variation. Am. Nat. 89: 151-158. ROBERTSON, A., 1959a Experimental design in the evaluation of
CLAYTON, G. A,,andA. ROBERTSON,1957 Anexperimental genetic parameters. Biometrics 15: 219-226.
check on quantitative genetical theory. 11. T h e long-term ef- ROBERTSON,A,,1959bThesamplingvariance of thegenetic
fects of selection.J. Genet. 55: 152-170. correlation coefficient. Biometrics 15: 469-485.
CLAYTON, G. A,, and A. ROBERTSON, 1964T h e effects of X-rays ROBERTSON,A,,1960 Atheoryoflimits in artificialselection.
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7
ROBERTSON, A., and J. M. RENDEL,1954 T h e performanceof
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SHRIMPTON,A.E., and A. ROBERTSON,1988a The isolation of
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