Immunology Today, VoL 9, No. 2, 1988

Construction of the map also depends on recombination analysis, genomic cloning, studies of deletion mutants etc. References to these procedures may be found in the publications cited.

John Trowsdale is in the Human Immunogenetics Laboratory, PO Box 123, Lincoln's Inn Fields, Imperial Cancer Research Fund, London WC2A 3PX, UK;

R. Duncan Campbell is in the MRC Immunochemistry Unit, Department of Biochemistry, Oxford OXl 3QU, UK.

References 1 Dunham, I., Sargent, C.A., Trowsdale, J. and Campbell, R.D. (1987)Proc. NatlAcad. Sci. USA 84, 7237-7241

2 Carroll, M.C., Campbell, R.D., Bentley, D.R. and Porter, R.R. (1984) Nature 307, 237-241 3 Carroll, M.C., Katzman, P., Alicot, E.M. etal. (1987) Proc. Natl Acad. Sci. USA 84, 8535- 8539 4 Hardy, D.A., Bell, J.l., Long, E.O., Lindsten, T. and McDevitt, H.O. (1986) Nature 323, 453-455 5 Inoko, H. and Trowsdale, J. (1987)Nucleic Acids Res. 8957-8962 6 Lawrance, S., Smith, C.L., Srivastava, R., Cantor, C.R. and Weissman, S.M. (1987) Science 235, 1387-1390 7 Ragoussis, J., Bloemer, K., Weiss, E.H. and Ziegler, A. Immunogenetics (in press) 8 Ragoussis, J., van der Bliek, A., Trowsdale, J. and Ziegler, A. (1986) FEBSLett. 204, 1-4

Mechanisms of B Cell Neoplasia 1987

The Basel Institute for Immunology in Switzerland has recently published an account of the Workshop on Mechanisms of B Cell Neoplasia held at the institute on 25-27 March 1987. Organized by Fritz Melchers and Michael Potter, the workshop was the fifth in a yearly series held alternately in Basel and at the National Institutes of Health in 8ethesda. The book can be obtained free of charge from the Basel Institute, although only a small number of copies are available.

Nobel Prize for immunologist E r r a t u m

The Japanese immunologist Susumu Tonegawa has been awarded the 1987 Nobel Prize for Physiology or Medicine. The prize is recognition for Tonegawas's pioneering work in the late 1970s on the generation of antibody diversity in the immune system - most notably the demonstration that separate genes encode the variable and constant regions of immunoglobulin molecules (Proc. NatlAcad. Sci. USA, 1976, 73, 3628). Tonegawa's contribution had been honoured a matter of weeks earlier, when he shared a Lasker prize with Philip Leder and Lee Hood, who also played major roles in elucidating the mechanisms responsible for generating antibody diversity. While. the bulk of his work on antibodies was performed at the Basel Institute in Switzerland, Tonegawa is currently at the Massachusetts Institute of Technology, and is now investigating the molecular genetics of T-cell receptor genes.

We apologise to Gillian Harcourt and Andy Jermy for an error which slipped into their article in our November issue 'Mapping the autoimmunizing epitopes of acetylcholine receptors' (ImmunoL Today, 1987, 8, 319-321). In Fig. 1, the binding sites of acetylcholine and oL-bungarotoxin are in a light tint (not a dark tint as originally stated) and the main immunogenic regisn is in a dark tint (not a light tint as originally stated) . . . . .

Strategies for codon usage in human VH families

Table 1. Human Ig variable region genes analysed

Sir, Although codon usage varies in vHI different gene families, the mechan- vHII ism underlying the evolution and VHIII maintenance of these differences is vHIV unknown. Grantham and Perrin (Im- munoL Today 7, 160-162, 1986) reported that the proline codon CCC was rare in Ig variable region (V) genes. We have recently found that the codon usage in functional and nonfunctional human variable re- gion genes of the heavy chain (VH), codons - ! 9 tO +94 (numbering according to Ref. 1) (Table 1, se- quences from Refs 1-12), differs from that reported by Grantham and Perrin most notably in proline codons. Our study gave frequencies of 0.11 (0.04 in Grantham and Per- VHSUbgro rin's report) for CCG, 0.29 (0.48) for CCA, 0.32 (0.46) for CCT and 0.28 _ (0.02) for CCC. VHI

This discrepancy derives from the v, II VH III

fact that the different human VH V, lV families (defined by sequen,-e homology 2) differ significantly in Numbers

VH subgroup Total no. No. of No. of nf nen~ nc;p.elnn~n~ f Jnrfinn~! segments a studied sequences

used

23 6 4 8 0 1 30 6 5 9 0 9

aFrom Refs 2 and 4

codon usage, and that Grantham and Perrin had not included the novel family (VH IV). The two exam- ples of codon usage which showed the most marked discrepancies (Cys and Pro) are given in Table 2. Similar differences exist for Thr, lie, Arg and Leu codons (data not shown). The pseudogenes followed the family

usage pattern, but were excluded from the calculations. The clear dif- ferences between the VH family codon usages suggests that various VH genes cannot be treated as a homologous group.

The largest human family, VH III, is less homologous within the family than, for instance, VH IV, but exclu- sively uses the TGT codon for Cys. The other human VH families and most mouse variable genes use TGC and TGT at about equal frequencies and the constant region genes strongly prefer TGC. Furthermore, the mouse VH family $107 shows the same TGT preference as VH III, and both families have conserved TGT codons at the same positions ( -1 , +22 and +92).

A preliminary study on mouse VH

Table 2. Cysteine and proline codons in human VH subgroups

roup Cys TGT TGC CCG

Pro CCA CCT CCC

4(0.44) 5(0.56) 1(0.08) 1(0.08) 9(0.75) 1(0.08) 2(0.67) 1(0.33) 1(0.20) 1(0.20) 2(0.40) 1(0.20)

15(1.00) 0(0.00) 1(0.08) 5(0.42) 6(0,50) 0(0.00) 10(0,48) 11(0.52) 6(0.11) 17(0.32) 9(0.17) 21(0.40)

in parentheses indicate prc, p0rtion of total c0d0n usage 35