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Simple inheritance of key traits distinguishing maize and teosinte
M O N I T O R
The SH3-domain protein Bemlp coordinates mitogen.activated prote.;n kiaase cascndc activation with cell cycle contr,'t In Sacc~aeomycesceee~Islae D.M. LYONS~TAI. Mol. Cell. BioL 16, 4095-4106 In file prelude to mating, hudding yeast resl×mdiog to mating pheromone activate a LXIAPkilxl~e C l y d e , accompanied by n e w gene expression. G1 cellcycle arrest and development of a 'shm~m'-Iike projection towards the mating partner. Accumulating evidence is re~x:aling a very c l o ~ interp"lay between these events. Lyons etal. looked for dosage suppressors of the G 1 arrest
Simple inherit~ce of key traits distinguishing maize and teosiate V.M,SZABOANDB. BURR MOL Ge~t. GeIleL 2":,2, 33-41 Maize w~ts first cultivated by native American farmers in Southern Mexico less than 10000 years ago. Its progenitor is widely helie,,~ed to be an annual teosinte that. while genetically similar to maize, is morphologically very different. l low, then, did m(xlem maize arise in such a short time? ~ilte answer seertxs
A double-strand break within a yeast artificial chromosome (YAC) containing human DI~Acan result in YACloss, deletion, or cell lethality t~.lLBENN+eTIT,T.L ','~'i~S~'MO+I~I~MX J.R. SNIPEANt) M.A.RE~XlCK Mol, Cell, Bird, lfi, 441'4-4425 A n o ~ l model sy,~e n t thr analyslr~g the consequences of introducing a single double-strand break (DSI?,}into human DNA comained wiflfin a }~asl artificial chromosome (YAC) is descdlx'd by 13cnnett et al, "II"~emultiple .4hi repeats within Ihe YAC were targeted for homologous recombination by tran.~formation of a YAC-comaining yeast strain with a plasmid harbouring an A l e repeat. As this plasmid also conrained the r~ognition site for the H e endonuclease (the YZ junction), plus tile b~A3 marker, the net result of this strateg-/was tile gene~ltion of a series of sir:tins containing H e recognition
defect caused by mutatiun in the g~ale for the MAP kinase, FUS3. One suppresser, BF~II1. was previously s h o w n to be required for morphological changes during hud emergence and shmoo formation. B ~ I I was almost as potent a suppressor as FAR1, the cyclin-Cdk inhihitor that medkltes the cell-cycle arrest. This was not due to toxicity, becatt~ BEM1 trintantS were defective in signal tmnsduction measured by G I arrest and transcdptlonal activation, whereas overexpression of B/~I1 slimulated signal ~msduction under a variety of condifioms. Genetic evidence placed ,?R~/I upstream of FUS3. and B I ~ f l interacted with STES. encoding the MAP kinase scaffold protein. in a two-hybrid interaction a,~say.
Components of the kinase c~scade copurified with B e m l p w h e n Ste5p was overexpressed. Although the evidence suggests BI:MI exerts its effect through stimulation of the MAP kinase cascade, in one FUS3 mutant, Bl~dl supp~ssed the G | arrest defect while hardly increasing tmn~'ription, sn how does B~3~I1 stimulate G1 arrest? BEMI required FARI to mediate cell-cycle arres~ and the two proteins were shown to interact. Previously identified sequence similarity between SteSp and Farlp might suggest B e m l p regulates these proteins by a common mechanism, having a dual role to stimulate signal transduction and cell-cycle atTeSt through direct interactions with SteSp and Farlp, respectively.
to be that the laige morphological differences are the preduct of rather few genes. In a maize-~en~inte cross, patenud plant t).pes are recovered in an F2 population with r~sunalfle frequentT ~) mendelkm segregation nlleS indicate that ahout five major genetic loci with large effects account for the differences, With the advent of good genetic maps of maize based on RFLPs tile race was o n to locate these loci. This paper recttses on the ardtite~aure of the male and femaleflowcrsand, aswithsimilarwork t?om other groulxs, the authors agree tidal relath'ely few loci are responsible
for the differences, the problem is that not everyone agrees as to which loci or to their relative importance. Part of the re0.~on fo,'flle d i s h , panties may lye tt~'hnit+al(discussed at some length in this paper), and while each of tile identified kxi could contain s ~ e m l gclles it shotlld be rememhered that homeotic genes denl0nstrate that single genes can have large pleiotropic effects o n plant form. x~11enthe few loci governing the differences in architeclure lydween maize and t t ~ i n t e are finally dis,secled the betting is that their effects will he resolved into single genes within them.
sites clc~se to several Ah~ repeals. [uduction of I)SBs was then achieved by expression of H e from a galactoscinducible prt~moter, in most cases, tile induced DSB ',~ls rapidly lepaired by recomhination between Aft/relveat sequences distal to the DSB. with consequenl loss of die eRA3 marker. IIowever, in a few cast's, the ll.':,B persisted, pedlaps hecause its dlrOtnt~sonlal Incation dkl not pemlit r~:ombinatkmal repair. In these cases file persistence of the DSB within tile non-essential YAC was Iound to lead to veil death n'amy honm :liter tile 1)Sl] first appeared. Previously, the aulhors }lad introduced a non-essemial centrtmleric plasmid con* lainmg a YZ jtmtxlon into a difi~rent strain and ob~dned similar results. However. this earlier result could not he reproduced in thi.~ study, apparendy because tile linearlzed plasmid was n o w more rapidly degraded than in the strain previously used, further emphasizing the importance of DSB persistence. Cells in which the DSB signal
persisted also underwent a prokmged G2 mrcsL (A previous observation delnonSlmTt~ I thai deler~tm nf the RAD9 checkpoint gene p~rtlally attenuated the observed letlxdity.) Thus, the authors conclude thai for a DSB to cause lethality it musl persist in the cell ned pethaps signal through the checkpoint appaRItus. They propose that targets h,r this mechanism might include checklmint kina.~s, DNA repair s~,~stcnls or die chrOlllOfiomal Segl'e.~ation aplyaratus. Finally, they point out parallels with the dependency of mdiationinduced cell-cy,.'le arrest and apoptofie lethality o n p53 in nxlmmafian ceils. ,¢~
"['l{.i NOVEMBER1996 VOL. 12 NO. 11 462
MoMtor cotttrlbuiors this month David Shema~,Diethard Tautz, Stephen Wilson, Simon DowelL Robert Slfiel~. Noel Lowndes and Debbie Morrison
The SH3-domain protein Bemlp coordinates mitogen.activated prote.;n kiaase cascndc activation with cell cycle contr,'t In Sacc~aeomycesceee~Islae D.M. LYONS~TAI. Mol. Cell. BioL 16, 4095-4106 In file prelude to mating, hudding yeast resl×mdiog to mating pheromone activate a LXIAPkilxl~e C l y d e , accompanied by n e w gene expression. G1 cellcycle arrest and development of a 'shm~m'-Iike projection towards the mating partner. Accumulating evidence is re~x:aling a very c l o ~ interp"lay between these events. Lyons etal. looked for dosage suppressors of the G 1 arrest
Simple inherit~ce of key traits distinguishing maize and teosiate V.M,SZABOANDB. BURR MOL Ge~t. GeIleL 2":,2, 33-41 Maize w~ts first cultivated by native American farmers in Southern Mexico less than 10000 years ago. Its progenitor is widely helie,,~ed to be an annual teosinte that. while genetically similar to maize, is morphologically very different. l low, then, did m(xlem maize arise in such a short time? ~ilte answer seertxs
A double-strand break within a yeast artificial chromosome (YAC) containing human DI~Acan result in YACloss, deletion, or cell lethality t~.lLBENN+eTIT,T.L ','~'i~S~'MO+I~I~MX J.R. SNIPEANt) M.A.RE~XlCK Mol, Cell, Bird, lfi, 441'4-4425 A n o ~ l model sy,~e n t thr analyslr~g the consequences of introducing a single double-strand break (DSI?,}into human DNA comained wiflfin a }~asl artificial chromosome (YAC) is descdlx'd by 13cnnett et al, "II"~emultiple .4hi repeats within Ihe YAC were targeted for homologous recombination by tran.~formation of a YAC-comaining yeast strain with a plasmid harbouring an A l e repeat. As this plasmid also conrained the r~ognition site for the H e endonuclease (the YZ junction), plus tile b~A3 marker, the net result of this strateg-/was tile gene~ltion of a series of sir:tins containing H e recognition
defect caused by mutatiun in the g~ale for the MAP kinase, FUS3. One suppresser, BF~II1. was previously s h o w n to be required for morphological changes during hud emergence and shmoo formation. B ~ I I was almost as potent a suppressor as FAR1, the cyclin-Cdk inhihitor that medkltes the cell-cycle arrest. This was not due to toxicity, becatt~ BEM1 trintantS were defective in signal tmnsduction measured by G I arrest and transcdptlonal activation, whereas overexpression of B/~I1 slimulated signal ~msduction under a variety of condifioms. Genetic evidence placed ,?R~/I upstream of FUS3. and B I ~ f l interacted with STES. encoding the MAP kinase scaffold protein. in a two-hybrid interaction a,~say.
Components of the kinase c~scade copurified with B e m l p w h e n Ste5p was overexpressed. Although the evidence suggests BI:MI exerts its effect through stimulation of the MAP kinase cascade, in one FUS3 mutant, Bl~dl supp~ssed the G | arrest defect while hardly increasing tmn~'ription, sn how does B~3~I1 stimulate G1 arrest? BEMI required FARI to mediate cell-cycle arres~ and the two proteins were shown to interact. Previously identified sequence similarity between SteSp and Farlp might suggest B e m l p regulates these proteins by a common mechanism, having a dual role to stimulate signal transduction and cell-cycle atTeSt through direct interactions with SteSp and Farlp, respectively.
to be that the laige morphological differences are the preduct of rather few genes. In a maize-~en~inte cross, patenud plant t).pes are recovered in an F2 population with r~sunalfle frequentT ~) mendelkm segregation nlleS indicate that ahout five major genetic loci with large effects account for the differences, With the advent of good genetic maps of maize based on RFLPs tile race was o n to locate these loci. This paper recttses on the ardtite~aure of the male and femaleflowcrsand, aswithsimilarwork t?om other groulxs, the authors agree tidal relath'ely few loci are responsible
for the differences, the problem is that not everyone agrees as to which loci or to their relative importance. Part of the re0.~on fo,'flle d i s h , panties may lye tt~'hnit+al(discussed at some length in this paper), and while each of tile identified kxi could contain s ~ e m l gclles it shotlld be rememhered that homeotic genes denl0nstrate that single genes can have large pleiotropic effects o n plant form. x~11enthe few loci governing the differences in architeclure lydween maize and t t ~ i n t e are finally dis,secled the betting is that their effects will he resolved into single genes within them.
sites clc~se to several Ah~ repeals. [uduction of I)SBs was then achieved by expression of H e from a galactoscinducible prt~moter, in most cases, tile induced DSB ',~ls rapidly lepaired by recomhination between Aft/relveat sequences distal to the DSB. with consequenl loss of die eRA3 marker. IIowever, in a few cast's, the ll.':,B persisted, pedlaps hecause its dlrOtnt~sonlal Incation dkl not pemlit r~:ombinatkmal repair. In these cases file persistence of the DSB within tile non-essential YAC was Iound to lead to veil death n'amy honm :liter tile 1)Sl] first appeared. Previously, the aulhors }lad introduced a non-essemial centrtmleric plasmid con* lainmg a YZ jtmtxlon into a difi~rent strain and ob~dned similar results. However. this earlier result could not he reproduced in thi.~ study, apparendy because tile linearlzed plasmid was n o w more rapidly degraded than in the strain previously used, further emphasizing the importance of DSB persistence. Cells in which the DSB signal
persisted also underwent a prokmged G2 mrcsL (A previous observation delnonSlmTt~ I thai deler~tm nf the RAD9 checkpoint gene p~rtlally attenuated the observed letlxdity.) Thus, the authors conclude thai for a DSB to cause lethality it musl persist in the cell ned pethaps signal through the checkpoint appaRItus. They propose that targets h,r this mechanism might include checklmint kina.~s, DNA repair s~,~stcnls or die chrOlllOfiomal Segl'e.~ation aplyaratus. Finally, they point out parallels with the dependency of mdiationinduced cell-cy,.'le arrest and apoptofie lethality o n p53 in nxlmmafian ceils. ,¢~
"['l{.i NOVEMBER1996 VOL. 12 NO. 11 462
MoMtor cotttrlbuiors this month David Shema~,Diethard Tautz, Stephen Wilson, Simon DowelL Robert Slfiel~. Noel Lowndes and Debbie Morrison