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 putative inhibitor of S-adenosylmethionine decarboxylase (SAMDC, EC 4.1.1.21) activity methylglyoxal(bis-guanylhydrazone) (MGBG) inhibited meristemoid/primordia formation while enhancing conjugated polyamine accumulation and ethylene 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 further examined the effect of 0.5 mM MGBG on the incorporation of labelled methionine into spermidine and spermine, on SAMDC transcript levels and activity and on putrescine oxidising (DAO) activity at different times in culture, MGBG-induced ethylene accumulation was also evaluated by gas chromatography (GC), In shoot-forming controls (grown on a medium supplemented with IAA + BA) label was mainly incorporated into free spermidine (82-86% of the total amount incorporated into pol! amines) while only 6-12% of radioactivity tvas recovered in free spermine, Some label was also found in putrescine, In the presence of MGBG, spermidine biosynthetic capacity was enhanced throughout 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 previous ones, suggest that MGBG, in fact, does not behave as a SAMDC inhibitor in shoot-forming tobacco thin layers and that its negative effect on organised growth is not due to SAMDC inhibition/polyamine depletion.