Methylglyoxal(bis-guanylhydrazone) inhibition of organogenesis is not due to S-adenosylmethionine decarboxylase inhibition/polyamine depletion in tobacco thin layers

Previous results indicated that in shoot-forming tobacco thin layers the pu tative inhibitor of S-adenosylmethionine decarboxylase (SAMDC, EC 4.1.1.21) activity methylglyoxal(bis-guanylhydrazone) (MGBG) inhibited meristemoid/p rimordia formation while enhancing conjugated polyamine accumulation and et hylene biosynthesis, thus showing an inverse relationship bet treen the two phenomena (Scaramagli et al, 1999), In order to better understand how MGBG causes polyamine overproduction and by using the same model system, ne fur ther examined the effect of 0.5 mM MGBG on the incorporation of labelled me thionine into spermidine and spermine, on SAMDC transcript levels and activ ity and on putrescine oxidising (DAO) activity at different times in cultur e, MGBG-induced ethylene accumulation was also evaluated by gas chromatogra phy (GC), In shoot-forming controls (grown on a medium supplemented with IA A + BA) label was mainly incorporated into free spermidine (82-86% of the t otal amount incorporated into pol! amines) while only 6-12% of radioactivit y tvas recovered in free spermine, Some label was also found in putrescine, In the presence of MGBG, spermidine biosynthetic capacity was enhanced thr oughout the culture by 28-45% compared with controls. The same occurred for spermine and putrescine, MGBG-enhanced spermidine synthesis was supported by increased SAMDC activity (days 1-2) and higher levels of SAMDC message ( days 1-7), On the contrary, the effect of the drug on putrescine oxidation was inhibitory starting from day 2, These results, together with the previo us ones, suggest that MGBG, in fact, does not behave as a SAMDC inhibitor i n shoot-forming tobacco thin layers and that its negative effect on organis ed growth is not due to SAMDC inhibition/polyamine depletion.