Blood Group and Serum Protein Differences in Some Central Australian Aborigines E

Blood Group and Serum Protein Differences in Some Central Australian Aborigines E. M. NICHOLLS,* H. B. M. LEWISt D. W. COOPER, AND J. H. BENNETT

Department of Genetics, University of Adelaide, South Australia. IN SEPTEMBER, 1962, as part of a study of some Australian aboriginal populations, blood samples were collected from various aboriginal groups in Cen- tral Australia. The early studies of Cleland (1926, 1930) and later investiga- tions (erg., Birdsell, 1950; Simmons et al., 1957) have drawn attention to the interesting variations in the frequencies of the blood types of the aborigines in this area. With the rapid increase lb recent years in the number of known genetic markers, not only for the red cell but more especially in serum proteins, further work on the serological characteristics of these people seemed desirable. Moreover, with the continuing drift of some populations from their old localities and the increased opportunity for relaxation of tribal affiliations, there is a need for further genetical work with these aboriginal populations with particular reference to what is known of their tribal groupings (cf. Bennett, 1963). The object of the present investigation was to study genetical variations among localities and also to explore the variation among tribes in Central Australia.

COLLECTION AND TYPING OF BLOOD SAMPLES Venesection was carried out using 10 ml. disposable plastic syringes. In each case, 1.5 ml. of blood was transferred to a specially prepared sterile phial containing Rous and Turner anticoagulant solution and the remainder was placed in a larger bottle and allowed to clot. After labeling, the bottles were placed in a box containing ice chips and sent to Alice Springs for dis- patch by air to Adelaide. Blood samples were collected at Alice Springs; at nearby Amoonguna; at Hermannsburg Mission, about 70 miles away in a west-southwesterly direction; at Areyonga, about 35 miles farther in the same direction; and at Pap- unya, about 130 miles in a west-northwesterly direction from Alice Springs (see Fig. 1). Altogether, blood was collected from 353 individuals. Twenty- one of these were recorded in the field as having some white ancestry. During the field investigation, a record was made of the tribe to which each individual (other than those having some white ancestry) said he belonged. The distribution of individuals by locality and reported tribal groupings is

Received December 14, 1964. fPresent address: Department of Human Genetics, University of New South Wales. tPresent address: Aberdeen and North-East of Scotland Blood Transfusion Service, Royal Infirmary, Aberdeen. 293 AMERICAN JOURNAL OF HUMAN GENETICS, VOL. 17, No. 4 (JULY), 1965 294 GENETIC STUDIES OF AUSTRALIAN ABORIGINES

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TABLE 1. THE DISTRIBUTION OF INDIVIDUALS BY LOCALITY AND TRIBE Anmat- Pitjand- Pin- Miscel- Tribe: Aranda jera Walpari Loritja jara tubi Kaiditj Ngalia laneous Total Locality: Alice Springs 4 1 1 - 9 - 2 - 2 19 Amoonguna 34 15 16 11 5 - 4 - 9 94 Hermannsburg 17 - - 22 6 1 - - 2 48 Areyonga 3 - 1 4 73 3 - - 2 86 Papunya 9 - 16 18 - 37 - 5 - 85 67 16 34 55 93 41 6 5 15 332 of blood type frequencies in these different tribal classes. Comparison of Table 1 with Fig. 1, which marks out the principal tribal areas (taken from the map published by Tindale, 1940) shows that the various local populations sampled in this study include a number of individuals far removed from their traditional tribal areas. Most of the red cell typings, using anti-A, -A1 (Dolichos biflorus), -B, -A+B, anti-M, -N, -S, -s, anti-P1, anti-C, -c, -D, -RhA, -E, -e, -hrs, anti-K, anti-Lea, -Leb, and anti-Fya, were carried out within three days of collection. The serum protein groupings were determined over a longer period using serum which had been stored at -30° F. The samples were typed for haptoglobin and transferrin constitution by starch gel electrophoresis. In addition, the Gm(a, b, x, c) and Inv(a) typings were determined by Dr. A. G. Stein- berg and these results, together with those for the Gc types obtained by Kirk, Cleve, and Bearn (1964), which these workers have kindly made available to us, are included here for completeness. RESULTS AND DISCUSSION The frequencies of the various blood types are shown in Tables 2 and 4, classified according to geographical localities and tribes, respectively. The corresponding gene frequencies are given in Tables 3 and 5. The results for the 21 part-white individuals are not included in these tables but are shown separately in Table 6. They will not be considered further in this article. Among the 332 blood samples from supposedly fullblood aborigines, there are seven where the presence of an unusual type raises the question of possible nonaboriginal ancestry. Five of these, all from Amoonguna, are Kell positive, and one from Papunya belongs to blood group B and is also Gm(b+ ). The seventh individual, also from Amoonguna, is the only other example of Gm(b+) in our material. Fullblood aborigines having blood group B or the Gm(b+) phenotype have not previously been reported from Central Aus- tralia, although both types are known in aborigines in the northeast of the continent and Gm(b+) is also found in the northwest. The Kell antigen has not previously been detected in fullblood aborigines. Some further in- vestigations were therefore indicated. Repeat blood samples were obtained and the Kell typings confirmed. Also, Mr. T. G. H. Strehlow of the University of Adelaide and Mr. D. A. Stewart of the Northern Territory Administration very kindly made further independent inquiries in the field as to possible nonaboriginal ancestry in these cases. No evidence was found to suggest 296 GENETIC STUDIES OF AUSTRALIAN ABORIGINES

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C4 C4 0 Lo C4 -h ZC4 cS oq l< NICHOLLS ET AL. 299 TABLE 8. ABO BLOOD GROUP FREQUENCIES IN CENTRAL AusTRALiAl Phenotype Tribe 0 A Total Number Aranda .38 .62 37 Anmatjera .31 .69 42 Walpari .30 .70 30 Loritja .34 .66 41 Pitjandjara .26 .74 102 Pintubi .29 .71 28 *From Campbell, Gray, and Hackett (1938). that these individuals are other than fullblood aborigines. The blood types of the seven individuals concerned are recorded separately in Table 7. They are also included in Tables 2 through 5. For the MN, Hp, Tf, and Gc groups, the frequencies given in Tables 3 and 5 have been obtained directly by counting genes. For the AO, P, Gm, and Inv groups, gene frequency estimates have been derived on the assumption that random mating frequencies obtain in the sample of individuals observed. The ABO Groups Only one individual belonging to blood group B was found (see Table 7), and, as in all earlier studies in Central Australia, there was no example of subgroup A2. The frequency of group Al individuals varies from about 0.50 at Alice Springs, Amoonguna, and Hermannsburg to 0.60 at Areyonga and 0.62 at Papunya, which is close to the highest value found in Australian aborigines. There is no significant heterogeneity in the frequency of A individuals between the five localities (x2 41 = 3.1, P = 0.6). In the tribal groups represented, the frequency of A individuals varies from 0.46-0.47 in the Aranda and Walpari, and up to 0.58-0.60 in the Loritja, Pintubi, and Pitjandjara, and 0.81 in the small sample of Anmatjera. There is no significant heterogeneity in respect to these frequencies among the six principal tribes represented (X2151 = 8.8, P = 0.13). While there is no significant over-all heterogeneity here, there is an apparent trend towards a higher A frequency as one moves into the desert populations west of Alice Springs. This is in agreement with earlier findings (cf. Campbell, Gray, and Hackett, 1936; Birdsell, 1950), though the change is less marked in our material. Although very little has been published on blood group frequencies in different tribes, some data on the tribal frequencies for the ABO blood groups in Central Australia were included in several of the early publications by Cleland and his colleagues. Perhaps the most extensive collection is that given by Campbell, Gray, and Hackett (1936). (See Table 8.) These data show a higher frequency of A than we have found, and this is most marked for the Aranda, Walpari, Pitjandjara, and Pintubi tribes. We may wonder to what extent departures from random sampling, differences between localities sampled, or changes of population with the passage of time have con- tributed to this difference. However, too much weight should probably not 300 GENETIC STUDIES OF AUSTRALIAN ABORIGINES be attached to these frequency differences, since the early data given by Campbell, Gray, and Hackett (1936), which were obtained from typings done in the field, show some very significant and unexplained discrepancies in A frequency between males and females in the same tribes. (The probabil- ity of obtaining by chance such an extreme discrepancy between the sexes as they found for the A blood group is 0.02 for each of the Aranda, Pitjand- jara, and Pintubi tribes. In their data, females show a marked excess of group A in the Pitjandjara and a deficiency in the-Aranda and Pintubi tribes.) The MNSs Groups All individuals reacted with anti-s but not with anti-S and so may be taken tobe homozygous for the gene s. The N gene frequency varies from 0.72 at Hermannsburg to 0.81 at Areyonga. The five localities do not show significant heterogeneity for this gene frequency (X2[4] = 5.5, P = 0.2), but a trend is apparent similar to that in group A frequency, with higher values at Areyonga and Papunya than elsewhere. Highly significant heterogeneity is encountered when the tribal groupings are considered (x2[5 = 23.2, P < 0.001). We may contrast the Pitjandjara, Pintubi, and Loritja, with N gene frequencies between 0.80 and 0.85, with the Aranda and Anmatjera, with N gene frequencies of 0.69 and 0.56, respectively, while the Walpari tribe has an intermediate value of 0.75. The trend towards a higher frequency of N in the desert tribes is in agreement with earlier findings, but the increase found here is not nearly as great as that described by Birdsell (1950). When the observed frequencies of the three M-N types are compared with their expected values calculated on the assumption of random mating within localities, the only locality to give a significant difference is Amoonguna (x2[ll= 10.2, P = 0.002). This is the locality with the greatest number of different tribes represented. There is close agreement between the random mating expectations and the observed genotypic frequencies for each of the five major tribal groupings. The P Groups The frequency of P1-positive individuals varies from 0.18 at Papunya to 0.30-0.32 at Amoonguna and Alice Springs. While there is not significant heterogeneity in these frequencies at the different localities (X2[4] = 5.7, P = 0.23), there is highly significant heterogeneity when the tribal groupings are considered (x2 [5] = 31.8, P < 0.001). The frequencies of Pi-positive individuals vary from the extremely low value of 0.07 in the Pintubi and Loritja through 0.20 in the Pitjandjara to 0.33 in the Aranda, 0.38 in the Walpari, and up to 0.56 in the small sample of 16 members of the Anmatjera tribe. In the few published reports on P gene frequency in Australian aborigines, some of which may need confirmation, there is a large range of variation in the frequencies similar to that described here among tribes. The value of 0.23 for the frequency of Pi-positive individuals at Haast's Bluff (Simmons et al., 1957) is close to the value of 0.18 at nearby Papunya, while the values observed in the Alice Springs and Amoonguna samples, and especially in the NICHOLLS ET AL. 301 Anmatjera and Walpari tribes, approach the much higher frequency of 0.68 recorded by Simmons et al. (1954) for 93 aborigines from Yuendumu. If the large range of variation in P gene frequency in Central Australia and the Northern Territory is confirmed, this blood group system would seem to deserve much further study in this area. The Rh Groups As in all other studies of Australian aborigines, no blood sample was found which failed to react with anti-D serum. Tests for the agreement between the observed phenotypic frequencies at the E-e locus and those expected assuming random mating within localities give a significant result only in the case of Hermannsburg (X2[I] = 6.3, P = 0.01). There is close agreement between the observed frequencies and the expectations when random mating is assumed to hold within each of the tribal groups. For the C-c locus, the observed frequencies differ significantly from those expected with random mating for each locality (Amoonguna, x2I] = 8.9, P = 0.006; Hermannsburg, x2 = 4.9 P = 0.003; Areyonga, X2[I] = 8.4, P = 0.006; Papunya, X2Ill = 7.1, P = 0.009). The differences are less extreme when the comparisons are made within tribal groupings, but they are, nevertheless, significant in three tribes (Aranda, x2[l] = 4.5, P = 0.04; Loritja, x2Ill = 5.2, P = 0.02; Pitjandjara, x2Ill = 6.6, P = 0.01). We are unable to account for these peculiarities in our data though a possible explanation is misclassification of some cDE/cDE cells as C(+), resulting from the use of anti-C serum containing incomplete anti-D. In any event, the C-c typings cannot be regarded as satisfactory. Ac- cordingly, the Rh gene frequencies shown in Tables 3 and 5 refer only to the marginal frequencies for the E-e genes which have been determined directly by counting. There is no obvious pattern in the variation of the E gene frequency in our data. There is not significant heterogeneity in this frequency either by localities (x2 4) = 1.6, P = 0.8) or tribes (x2[5] = 0.7, P = 0.98). The observed frequencies are among the highest found in Australian aborigines. They may be contrasted with the following values for the E gene frequency given by Simmons (1958): 0.25 in 1,698 aborigines from Western Australia, 0.14 in 533 aborigines from Queensland, and 0.13 in 493 aborigines from the Northern Territory. At Haast's Bluff and Yuendumu, the respective frequencies 0.32 and 0.41 given by Simmons, Graydon, and Semple (1954) and Simmons et al. (1957) agree well with our figures. With one exception, all blood samples giving a positive reaction with anti-E were positive with the anti-ET antibody (discovered in an aborigine by Vos and Kirk, 1962). The exception was a member of the Aranda tribe at Amoon- guna. This is comparable with the frequency of one ET(-) among 99 E( +) aborigines in North Queensland reported by Vos and Kirk but is in marked contrast with their finding that in a sample of 208 aborigines from the Western Desert who reacted with European anti-E 35% were ET-negative. Typings with anti-hrs (Shapiro, 1960) were carried out on the 210 blood samples collected at Alice Springs, Amoonguna, and Papunya, and with one 302 GENETIC STUDIES OF AUSTRALIAN ABORIGINES exception these gave the same reactions as with anti-e. The exception was one member of the Pintubi at Papunya whose blood sample gave the reactions e(+) hrs(-), but we have been unable to obtain a second sample to confirm this result. With an anti-RhA serum, which had been tested with the red cells of Mrs. P. S. (Wiener, Geiger, and Gordon, 1957). all individuals were RhA-positive except for two members of the Aranda, one at Areyonga, and one at Papunya. The Kell Groups All blood samples failed to react with anti-K except for the five individuals from Amoonguna already mentioned (Table 7). The Lewis Groups The Lea antigen was not encountered at Areyonga, but Le( a+) individuals occurred with a frequency of 0.08 in the Hermannsburg sample, 0.04 in the combined Amoonguna-Alice Springs sample and 0.01 in the Papunya sample. This phenotype was present with a frequency of 0.07 in members of the Aranda tribe and 0.06 in the Anmatjera but rarely in the other tribes. In fact, only three other examples were found in the tribes being considered here, one each in the Walpari, Loritja, and Pitjandjara. Simmons et al. (1957) found no example of Le(a+) in 100 persons tested at Haast's Bluff, which is close to our result at nearby Papunya, and the frequencies found for Yuendumu in the Northern Territory and for Western Australia (Simmons, 1958) are very similar to our values for the Aranda. The anti-Leb antibody used was the usual kind which fails to react with most Al cells. The frequency of the Le(b+) phenotype in group 0 individuals varies from 0.65 at Areyonga and 0.77 at Papunya to 0.84 at Hermannsburg and 0.83 in the combined Amoonguna-Alice Springs sample with no significant over-all heterogeneity (X2[31 = 4.45, P = 0.22). In the tribal groups, the corresponding frequency varies from 0.72 in the Anmatjera and Aranda to 0.89-0.91 in the Walpari and Loritja and 0.70-0.76 in the Pitjandjara and Pintubi with significant heterogeneity between these three classes (x2 21 = 7.9, P = 0.02). These Le(b+) phenotypic frequencies are of interest in that they mark out the Walpari and Loritja tribes as different from the four other tribes which have very similar frequencies. There has been no previous re- port on the Leb antigen in Australian aborigines, but the high frequency of Le(b+) individuals is consistent with the very high frequency of secretors (97%) reported by Simmons, Graydon, and Semple (1954) in 77 individuals from Yuendumu. The Duffy Groups All red cell samples reacted positively with anti-Fya. This agrees with the results of all previous studies with this blood group in Australian aborigines. Haptoglobins The Hp' gene frequency varies from 0.03 in the small sample from Alice Springs to 0.29 at Hermannsburg. The five localities show significant het- NICHOLLS ET AL. 303 erogeneity for this gene frequency (x214] = 12.6, P = 0.014). When tribal differences are considered, the heterogeneity is more marked (X2 i,5 = 19.5, P = 0.003). A contrast is apparent between the Aranda, Anmatjera, and Lor- itja tribes on the one hand with values for the Hp' gene frequency varying between 0.25 and 0.31 and the Pitjandjara, Pintubi, and Walpari on the other with values in the range 0.11-0.18. The Hp' gene frequency has about the same range- of variation in these data as in those for Western Australia and Queensland (Kirk and Lai, 1961; Kirk, Lai, and Horsfall, 1962), and there seems to be a general tendency for the lowest values to occur in the central desert populations. Further evidence comes from the typings of 190 aborigines now living at Yalata in South Australia (Fig. 1) and said to belong mostly to the Pitjandjara tribe. These were found to be 0.03 Hp 1-1, 0.25 Hp 2-1, 0.72 Hp 2-2, giving a Hp' gene frequency of 0.15, in close agreement with the Pitjandjara series described above. Four examples of the Hp 0 phenotype were found, one in a member of the Ngalia at Papunya and three in members of the Loritja, of whom two were at Papunya and one at Hermannsburg. Two examples of the rare Johnson type haptoglobin were found at Papunya in members of the Pintubi tribe. The results of a follow-up family study in one of these cases will be reported elsewhere (Cooper, Lewis, and Nicholls, 1965). The observed frequencies of the haptoglobin types are in close agreement with the expected values assuming random mating either within localities or within tribes. There is a striking contrast between our results and the Hp' gene frequency of 0.63 reported by Budtz-Olsen (1958) for 100 aborigines from Central Aus- tralia. Two-thirds of the individuals sampled by Budtz-Olsen came from Alice Springs and the rest from Haast's Bluff, and they were said to be mostly from the Pintubi tribe. However, these early typings by Budtz-Olsen, determined by paper electrophoresis, probably are not reliable. Transferrins The frequency of the TfDI gene reaches the value 0.16 in the small sample from Alice Springs but otherwise varies within the range 0.05-0.10 for the remaining localities. There is no significant heterogeneity in these frequencies (x2[4] = 4.7, P = 0.32). There is also no significant heterogeneity in the TfDI gene frequencies for the different tribal groupings, where the values lie in the range 0-0.12 with no obvious trend (X2[5] = 8.7, P = 0.13). The TfD1 gene frequency has about the same range of variation in these data as in those for North Queensland (Kirk, Lai, and Horsfall, 1962). In Western Australia, the frequency of TfDI is somewhat higher with a maximum of about 0.20 in the Western Desert (Kirk and Lai, 1961). This is in contrast with the much lower values of 0.06 and 0.10 given here for members of the Pintubi and Pitjandjara tribes, respectively. However, the typing of the 190 blood samples from Yalata gave a frequency cf 0.32 for the TJD' gene, the phenotypic frequencies being 0.47 CC, 0.42 CD1, and 0.12 D1D1. In view of the large difference between this value and the frequency we have found in the Pitjandjara tribe and as the blood samples from Yalata, which had been 304 GENETIC STUDIES OF AUSTRALIAN ABORIGINES collected as part of a medical survey, had been stored for many months before being typed, these results deserve to be checked. The possibility that some of the D zones scored in the starch gels of these sera were due to re- moval of sialic acid by the enzyme neuraminidase cannot be excluded (Blum- berg and Warren, 1961). The Gm and Inv Serum Groups Typings for the gamma globulin groups Gm and Inv, carried out by Dr. A. G. Steinberg, showed that all samples were Gm(a+c-). Further, all samples were Gm(b-) except for one individual at Amoonguna and another at Papunya. (See Table 7.) The absence or near absence of the Gm(b+) phenotype in this material is in agreement with the finding by Vos, Kirk, and Steinberg (1963) that it was not present in 289 blood samples from the Western Desert and is in striking contrast with frequencies of 0.31 found by those authors in the Kimberley area of Western Australia and 0.22 reported by Flory (1964) in aborigines from North Queensland. The frequency of the Gm(x+) phenotype varies from 0.31 at Hermanns- burg to 0.47-0.51 at Alice Springs, Amoonguna, and Areyonga and up to 0.61 at Papunya with significant heterogeneity between localities (X214] = 11.2, P = 0.03). For the tribal groupings, the frequency of the Gm(x+) phenotype varies from 0.36 in the Aranda to values in the range 0.47-0.63 in the other tribes. However, there is no significant over-all heterogeneity between the six tribal groups in respect to these phenotypic frequencies (x2151 = 8.6, P = 0.13). These frequencies may be compared with the value of 0.47 reported by Vos, Kirk, and Steinberg (1963) for aborigines from the Western Desert. The frequency of the Inv(a+) phenotype also has its lowest value (0.19) at Hermannsburg and varies in the range 0.37-0.47 at the other centers with significant over-all heterogeneity between the five localities (X2[41 = 10.1, P = 0.04). For the tribal groupings, the frequency of the Inv(a+) phenotype varies from 0.56-0.58 in the Aranda and Anmatjera to values in the range 0.31-0.42 in the other tribes. The heterogeneity between these frequencies is almost sigiificant at the 5% level (x21fi = 10.7, P = 0.06). The Inv (a+) frequencies for the Pintubi and Pitjandjara tribes are somewhat lower than the value of 0.43 reported by Steinberg (1962) for aborigines from the Western Desert, while the higher frequencies in the Aranda and Anmatjera are close to the value of 0.52 reported by Flory (1964) in a sample of 103 aborigines from North Queensland. The Go Groups The typings for the group-specific component in this material (Kirk, Cleve, and Beam, 1965) show a very low frequency for the Gcs gene with no significant heterogeneity between localities or tribal groups. Among tribes this frequency varies from 0.04-0.06 for Aranda and Anmatjera to 0.07-0.11 for Wal- pari, Pintubi and Pitjandjara. The gene GcAb was encountered at Areyonga, Hermannsburg, and Amoonguna, the greatest frequency (0.05) being at Amoonguna. In the Aranda, this gene was found with a frequency of 0.07. NICHOLLS ET AL. 305

TABLE 9. FREQUENCIES OF THE A AND P1 BLOOD GROUP PHENOTYPES CLASSIFIED BY LOCALITY AND TRIBAL AFFILIATION Blood Group A Blood Group Pi Locality Locality Amoon- Hermanns- Pap- Amoon- Hermanns- Pap- Tribe guna burg unya Average guna burg unya Average Aranda .47 .47 .56 .46 .30 .35 .44 .33 Walpari .31 - .69 .47 .31 -- .38 .38 Loritia .64 .46 .65 .50 .09 .09 .06 .07 Average .52 .48 .63 .42 .19 .18

DISCUSSION This study, involving ten red blood cell or serum polymorphisms, has not only confirmed and extended earlier findings on the distinctiveness of gene distribution in the aborigines of Central Australia but also has revealed some large differences in gene frequencies between the populations in this area. There is a striking contrast between, on the one hand, the Aranda and An- matjera tribes from the ranges surrounding Alice Springs and, on the other hand, the Pintubi and Pitjandjara tribes from the desert to the southwest. The latter tribes are characterized by higher frequencies for the A, N, PF,, Hp', and Gm"t genes and for the Le(a-b-) and Inv(a-) phenotypes. On the basis of their gene frequencies, the Walpari and Loritja tribes would seem to occupy intermediate positions with a tendency for the Loritja to be somewhat closer to the desert tribes, although in the case of the Lewis groups, the frequency of the Le(b+) phenotype is significantly higher in the Loritja and Walpari samples than in those from the other tribes where it shows little variation. The two major groups of tribes which have been distin- guished in this way can also be contrasted ethnologically (Strehlow, 1965). The Pintubi and Pitjandjara tribes have gene frequencies for some of the polymorphisms, e.g. Hp, Gm, Gc, which are very similar to those for the more westerly tribes in the Western Desert but there seem to be some notable differences, e.g. Tf, Inv(a+). As the populations in the different localities include individuals from several tribes, the contrast in gene frequencies is not nearly so marked or, we think, meaningful when localities are made the basis of population comparison. If sufficient material could be obtained, it would be of interest to analyze gene frequency data, taking account of variation among localities and tribes as well as the possibility of a locality-tribe interaction. Our data are, of course, inadequate for this purpose, but it may be of interest to com- pare the frequencies found for the A and P phenotypes set out in two-way classifications for three of the major tribes and three localities (see Table 9). Such differences, if confirmed in larger samples, might suggest that tribal rather than geographical grouping is the more important factor in determin- ing P frequency, whereas, for the A frequency, locality might also be of some importance. The possibility that some of the known genetic polymorphisms reflect adaptation to particular habitats in this area is one which deserves further consideration. The extent of intertribal marriage under pres- 306 GENETIC STUDIES OF AUSTRALIAN ABORIGINES ent conditions in Central Australia and the part it is playing in changing gene frequencies in tribal and geographical populations also deserves further attention.

SUMMARY Blood samples from 353 Australian aborigines living at Alice Springs, Amoonguna, Hermannsburg, Areyonga, and Papunya in Central Australia have been typed for the ABO, MNSs, P, Rh, Kell (K), Lewis, and Duffy (Fya) blood groups and for haptoglobins, transferring, the group specific component (Gc), and the Gm and Inv serum groups. All but 21 of these individuals are thought to be fullblood aborigines. An unexpected finding was that five supposedly fullblood aborigines were Kell- positive, one was blood group B and Cm(a+b+c-x-), and another was Gm(a+b+c-x+). These results were unexpected since the Kell antigen has not previously been found in fullblood Australian aborigines, and neither blood group B nor the Gm(b+) phenotype has been encountered in fullblood aborigines in Central Australia. The variation in the frequencies of these blood groups or serum protein types is considered with respect to differences in locality and tribal affiliation. Dif- ferences in tribal affiliation are found to be closely associated not only with gene frequency differences between localities but also with the genetic variation within samples at the various localities. A striking contrast is evident between the set of gene frequencies in the Pintubi and Pitjandjara tribes, which have been centered in the desert area to the west of Alice Springs, and the Aranda and Anmatjera tribes, which have been centered in the ranges surrounding Alice Springs. The former tribes are characterized by higher frequencies for the A, N, Ps, and Hp2 genes as well as for the Le(a-b-), Gm(x+), and Inv(a-) phenotypes. The Walpari and Loritja tribes occupy intermediate positions as far as their gene frequencies are concerned, with a tendency for the Loritja to be somewhat closer to the desert tribes. With the Lewis groups, however, the frequency of the Le(b+) phenotype is significantly higher in the Loritja and Walpari samples than in those from the other tribes where it shows little variation. It is suggested that in further population surveys of Australian aborigines in Central Australia an attempt should be made to give more attention to studying tribal affiliation.

ACKNOWLEDGMENTS The assistance of members of the Department of Health and Welfare, Northern Territory, and of Lutheran missionaries at Hermannsburg, Areyonga, and Papunya is gratefully acknowledged. We are indebted to Mr. N. Z. Bahnisch for assistance in the field; to Dr. A. G. Steinberg for the Gm and Inv typings; to Dr. R. L. Kirk for the Gc typings; to Miss C. Oertel, who performed a number of the statistical computations; and, for gifts of antisera, to Dr. R. J. Walsh (anti-S), Dr. J. O'Riordan (anti-s), and Mr. G. H. Vos (anti-ET, anti-RhA, anti-hr", the last from Dr. M. Shapiro); to Mr. E. E. R. NICHOLLS ET AL. 307 Vincent and Mr. G. Knighton, who performed most of the blood group tests, and, above all, to the Australian Institute of Aboriginal Studies for financial assistance. REFERENCES BENNETT, J. H. 1963. Genetical and biometrical studies. In Australian Aboriginal Studies (O.U.P.) BIRDSELL, J. B. 1950. Some implications of the genetical concept of race in terms of spatial analysis. Cold Spring Harbor Symp. Quant. Biol. 15: 259-314. BLUMBERG, B. S., AND WARREN, L. 1961. The effect of sialidase on transferrins and other serum proteins. Biochim. Biophys. Acta 50: 90-101. BuDFZ-OLsEN, 0. E. 1958. Haptoglobins and haemoglobins in Australian aborigines. Med. J. Aust. 2: 689. CAMPBELL, T. D., GRAY, J. H., AND HACKETT, C. J. 1936. Physical anthropology of the aborigines of Central Australia. Oceania 7: 106-139. CLELAND, J. B. 1926. Blood grouping of Australian aboriginals. Aust. J. Exp. Biol. Med. Sci. 3: 33-5. CLELAND, J. B. 1930. Further results in blood grouping Central Australian aborigines. Aust. J. Exp. Biol. Med. Sci. 7: 79-89. COPER, D. W., LEwIs, H. B. M., AND NICHOLLS, E. M. 1965. Haptoglobin Johnson in the Australian aboriginal. (in press) FLORY, L. L. 1964. Serum factors in Australian aborigines from North Queensland. Nature 201: 508. KIRK, R. L., AND LAI, L. Y. C. 1961. The distribution of haptoglobin and transferrin groups in South and South East Asia. Acta Genet. Stat. Med. (Basel) 11: 97-105. KIRKu, R. L., LAI, L. Y. C., AND HORSFALL, W. R. 1962. The haptoglobin and transferrin groups among Australian aborigines from North Queensland. Aust. J. Sci. 24: 486-488. KIRK, R. L., CLEVE, H., AND BEARN, A. G. 1965. The distribution of GC types in sera from Australian aborigines. Amer. J. Phys. Anthrop. (in press). SHAPIRO, M. 1960. Serology and genetics of a new blood factor hrs. J. Forensic Med. 7: 96-105. SIMMONS, R. T., GRAYDON, J. J., AND SEMPLE, N. M. 1954. A blood group genetical survey in Australian aborigines. Amer. J. Phys. Anthrop. 12: 599-606. SIMMONS, R. T., SEMPLE, N. M., CLELAND, J. B., AND CASLEY-SMITH, J. R. 1957. A blood group genetical survey in Australian aborigines at Haast's Bluff, Central Aus- tralia. Amer. J. Phys. Anthrop. 15: 547-554. SIMMONS, R. T. 1958. A review of blood group gene frequencies in aborigines of the various Australian states. Proc. 7th Cong. Internat. Soc. Blood Transf., pp. 287-292. STEINBERG, A. G. 1962. Progress in the study of genetically determined human gamma globulin types (The Gm and Inv groups). Prog. Med. Genet. 2: 1-33. STREHLOW, T. G. H. 1965. Culture, social structure and environment in aboriginal Central Australia. In Aboriginal Man in Australia. Sydney: Angus and Robertson. TINDALE, N. B. 1940. Distribution of Australian aboriginal tribes: a field survey. Trans. Roy. Soc. So. Aust. 64: 140-231. TINDALE, N. B. 1953. Tribal and intertribal marriage among the Australian aborigines. Hum. Biol. 25: 169-190. Vos, G. H., AND KIRK, R. L. 1962. A "naturally occurring" anti-E which distinguishes a variant of the E antigen in Australian aborigines. Vox Sang. 7: 22-32. Vos, G. H., Knuc, R. L., AND STEINBERG, A. G. 1963. The distribution of the gamma globulin types Gm(a), Gm(b), Gm(x), and Gm-like in South and Southeast Asia and Australia. Amer. J. Hum. Genet. 15: 44-52. WIENER, A. S., GEIGER, J., AND CORDON, E. B. 1957. Mosaic nature of the Rho factor of human blood. Exp. Med. Surg. 15: 75-82.