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3 Bistis, G.N. (1983) Exp, Mycol. 7, 292-295 4 Herskowitz, I. (1988) Microbiol. Rev. 52, 536--553 5 Perkins, D.D., Radford, A., Newmeyer, D. and

Bjorkman, M. (1982) MicrobioL Rev. 46, 426--570 6 Mortimer, R.K., Contopoulou, C.R. and King, J.S. (1991) in

The Molecular and Celhdar Biology of the Yeast Saccbaromyces (Vol. 1) (Broach, J.R., Pringle, J.R. and Jones, E.W., eds), pp. 737-812, Cold Spring Harbor Laboratory Press

7 Lennon, G.G. and Lehrach, H. (1992) Curt. Ge~et. 21, 1-11 8 Ainsworth, G.C. (1973) in The Fungi: An Advanced

Treatise(Vol. IVB)(Ainsworth, G.C., Sparrow, F.K. and Sussman, A.S., eds), pp. 1-7, Academic Press

.9 Berbee, M.L. and Taylor, J.W. (1992)Mol. Biol. Evol. 9, 278-284

10 Kues, U. and Casselton, L.A. (1992) Mycol. Res. 96, 993-1006

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Growth, Differentiation and Sexuality (Vol. I) (Wessels,J.G.H. and Meinhardt, F., eds), pp. 295-306, Springer-Verlag

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17 Debuchy, R., Arnaise, S. and Lecellier, G. (1~)3) Mol. Gen. Genet. 24 l, 667-.-673

18 Astell, C.R. etal. (1981) C~'1127, 15-23 19 Kelly, M. et al. (1988) P~IBOJ. 7, 1537-1547 20 Jantzen, H-M, Admon. A., Bell, S.P. and Tji:m, R. (1990)

Nature 344,830---836 21 Sinclair, A.H. et al. (1990) Nature 346, 240-244 22 Scott, M.P., Tamkum,J.W. and Hatzell, G.W. (1989)

Biochim. Biophys. Acta989, 2"3-48 23 Giniger, E. and Ptashne, M. (1987) Nattlre330, 670~72

24 Herskowitz, I. (1989) Nature342, 749--757 25 Phitley, M.L. and Staben, C. (1994) Genetics 137, 715-722 26 Metzenberg, R.L. (1990) Genetics 125, 457--462 27 Zickler, D. et al. (1995) Genetics 140, 493-503 28 Herskowitz, I., Rine, J. and Strathern, J. (1992) in The

Molecular and Celhdar Biology of the Yeast Saccbammrces(Vol. 2)( Jones, E,W., Pringle, J.R. and Broach, J.R., eds), pp. 583--656, Cold Spring Harbor Laboratory Press

29 Klar, AJ.S. (1992) in The Molecular and Cellular Biology of the Yeast Saccba~myces(Vol. 2)(Jones, E.W., Pringle, J.R. and Broach, J.R., eds), pp. 74%777, Cold Spring Harbor Laboratory Press

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31 Kurischko, C. et aL (1992) Mol. Gen. Genet. 232, 423--426 32 Perkins. D.D. (1987) Genetics 115, 215-216 33 Rt,~,lriguez, R.J. and Owen, J.L. (1992) Exp. Mrcol. 16,

291-301 34 Duntze, W., Betz, R. and Nientiedt, M. (199,D in "/'he

Mycota. Growth. Differentiation and &:vuality(Vol. I) (Wessels, J.G.H. and Meinhardt, F., eds), pp. 382-399, Spnnger-Verlag

35 Champe, S.P. and El-Zayat, A.A.E. (1989).L BacterioL 171, 3982-3988

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Res. 97, 485--496 38 Gooday, G.W. (1994) in lbe Mycota. Growth,

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39 Ndson, M.A. and Metzenberg, R.L. (1992) Genetics 132, 149--162

I MdL NELSON (manelson@trttogunntedu) is 1N THE LJEPARTMENT OF BIOLOGY) UNIVERSn'g OF NEW MF.XiC~ ALnU~UER~ NM 87131, USA-

M E E T I N G R E P O R T S

Signals to green SIGNALING IN PI..M~' DEV1ELOPMENT, tOLl) SI'I~.ING HARBOR I.MLORATORY, USA, 27 Si':tq'V.MBER--I O ~ o m ! H 1995.

Significant progress in the plant sig- naling field was reported at a very successful meeting. The following areas were covered: germination, photo morphogenesis, hormone sig- nal transduction, meristem formation, cell--cell interactions, flowering, pol- lination and fertilization, embryogen- esis and plant -pathogen interactions.

The organizers had specifically chosen chairpeople from varied spe- ciality areas so that the audience was exposed to a wide range of ap- proaches and techniques varying front sequence information of regu- latory genes to striking enhancer- or

gene-trap pattern.,; in the ovule (U. Grossniklaus, CSH) to a video of in vitro fertilization of maize gametes (N. Leduc from the Dumas laboratory, Lyon). The molecular genetic analy- sis of a wide range of processes had clearly moved the field ahead considerably and put meat on the bones of many genetic pathways.

The two fields that had shown most progress were light signal trans- duction and p lan t -pa thogen inter- actions, Impressive progress was reported on the analysis of COP1 and interacting proteins (CIP loci; M. Matsui, Deng laboratory, Yale),

TIG FEBRUARY 1996 VOL. 12 NO. 2

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and suppressor loci: SOP and HY5 (L. Ang, Deng lahoratory, Yale). The pathogen field has been united by the featt, re that the majority of disease- resistance genes, isolated from a diverse range of plants and confer- ring resistance to fungi, viruses and bacteria, encode proteins containing leucine-rich repeat motifs (LRRs) and either contain, or are likely to interact with, other proteins containing kinase domains.

Other key areas are open ing up with the cloning of genes in- volved in: gibberel l in signaling, SPY (N. Olzewski, Minnesota) and

M E E T I N G R E P O R T S

GAI (P. Leroy, Harberd laboratory, Norwich); auxin transport RCN1 (A. DeLong, Soil laboratory, Yale) and TIR1 (another LRR-containing protein; L. Hobble, Estelle labora- tory, Bloomington); and the control of flowering time - the alternatively spliced Arabidopsis FCA gene. which encodes a protein containing RNA-binding domains (C. Dean, Norwich), and the maize 119 gene. which encodes a Zn-finger-contain- ing protein (J. Colasanti, Sundaresan laboratory, CSH). Evidence was pre- sented to support the idea that ID does not work in a cell autonomous manner, reminding one of 'florigen'. the graft-transmissible floral-promot- ing substance proposed in 1937.

Genes controlling shoot meristem formation and maintenance in Ara- bidopsis, STMI (encoding a homeo- domain protein), TPL and PNH

(K. Barton, Wisconsin) were de,,m'ribed. STM1 was shown to interact with CLV1 (S. Clark, Ann Arbor), another LRR-containing protein. KNOTFED 1, a maize homeodomain protein in- volved in specifying cell fate non- cell-autonomously, was shown to move between cells through plasmo- desmata (D. Jackson, Hake labora- tory, Albany, California). The KN1 protein also co-transported the KN1 RNA through the plasmodesmata. P. Becraft (McCarty laboratory, Gainsville) discussed a maize mutant, crinkly leaf4, in which epidemlai cells from adjacent leaves coalesce. This gene encodes a protein with characteristics of a receptor kinase.

There were a few surprises too: the DET2 locus (im,oh,ed in the negative regulation ofphotomorpho- genesis in the dark) was shown to encode a protein with homology to

a steroid reductase, thus, opening up the possibility of the involvement of brassinosteroid hormones in ligh: regulation (J. Li, Chary laboratory, La Jolla). Also, the r~aize DK$-Sgene (a mutation in wMch blocks the formation of the .~hoot meristem) encodes a protein with homology to coproporphyrinogen oxidase (C, Rivin, Oregon State), It will be inter- esting to establish how a block in tetrapyrrole synthesis leads to loss of all the components of the embryonic shoot system.

Many participants also had one more lesson to learn - how to eat the mandatory lobster!

Caroline Dean arabid0psis@bbsrc.ac.uk

Jobn hines Centre, Colney Lane, Nomqcb, UK NR4 7UH.

European geneticists merge disease ~ O DISORDF.KS AND ~ GENTS IN

About 120 scientists came to the Costa Brava coast to attend this European research conference, which was co- sponsored by the European Science Foundation and the Eumconferences Activity of the European Union. The Mediterranean made a memorable backdrop to our discussions, carried out both in the meeting room and on the terrace for coffee breaks in the mild autumn sunshine.

The aim of the meeting was to bring together geneticists of various s t r i p e s - clinical, molecular, popu- latkm and anthropological - to talk to each other about genetic diversity. both normal and disease-related, and introduce concepts, prohlems and analytical techniques from each area of research to this wider audience. A further motivation was to encourage development in the new multi- disciplinary research are.a of genetic epidemiology.

We began by hearing sevend presentations on the evolutionary history of European populations, inferred fi'om mitochondrial (mr) DNA and classical blood polymor- phisms. Except for the distinction of the Saami of northern Scandinavia, European populations are remark- ably homogeneous. "lk) the extent that

DIFF~REqr EUROPEAN IIOPIIIATIONS, SAN FELIt"

there is variation, the main patterns are dines, interpreted to reflect migr- ation and dispersal of Middle Eastern farmers during the Neolithic period (4000-8000 years before present). However, there is some difficulty rec- onciling this interpretation with the absence or low frequency in Europe of mtDN~, lineages common to the Middle I '-a:~t, Futthemmre, a time-depd~ of roughly 40000 years estimated from mtDNA indicates a Paleolithic origin fi~r European diversity.

Unl:,~e nonnal diversity, disease mutations for Mendelian disorders, such as cystic fibrosis and phenyl- ketonuria, show considerable popu- lation specificity, consistent with their recent origins within the last few fllou- sand years. Yet, even among them gen- etic variants is one, the cystic fibrosis allele AFS08, with an estimated age suggesting Paleolithic ancestry. Per- haps the high frequency of this allele is the result of a Paleolithic population expansion fi'om a small number of founders? Who might they have l~nen? Current interpretations of the data st, g- gest that European diversity derives from Africa rather than from local Neandertals. A common African origin has Ixeen accepted for normal diver- sit3,; will genetic diseases trace back to

TIG FEBRUARY 1996 VOl., 12 No. 2

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Africa also? Another question arises concerning selective advantage on het- erozygous carriers of dimase alleles. One viewpoint is fl~at extensive gen- etic drift in pre-Neolithic populations wiped out most selectively balanced polymorphisms, except at HLA, and it is only as population numbers lx~come large that selection kicks in. But when does a rece~ive allele, that is deleterious as a homozygous geno- type, seem t(a~ common (and too old) to be explicable without hetero- zygous advantage?

Anotller group of genetic diseases that attract considerable interest are those due to trinucleotide repeat expansions. Studies of flxese disea~s are characterized by dismissal lx~th of selection and of lx~pulation history, as important evolutionary forces, in order to concentrate on the dynamics of the mutation process. Whefl~er or not the details of the nlutation process ~m be correctly detem~ined widxout taking selection and population history into accxmnt is a moot point. The spread of alleles ",xtending into the disease range at these sevemt loci is as great or greater for Europeans compared with other populations, which is not easy to understand if European diversity was squeez~.M in a founder event, Also it is