Two Arabidopsis mutants that overproduce ethylene are affected in the posttranscriptional regulation of 1-aminocyclopropane-1-carboxylic acid synthase

Citation
Ke. Woeste et al., Two Arabidopsis mutants that overproduce ethylene are affected in the posttranscriptional regulation of 1-aminocyclopropane-1-carboxylic acid synthase, PLANT PHYSL, 119(2), 1999, pp. 521-529
Citations number
55
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT PHYSIOLOGY
ISSN journal
00320889 → ACNP
Volume
119
Issue
2
Year of publication
1999
Pages
521 - 529
Database
ISI
SICI code
0032-0889(199902)119:2<521:TAMTOE>2.0.ZU;2-J
Abstract
The Arabidopsis mutants eto1 (ethylene overproducer) and eto3 produce eleva ted levels of ethylene as etiolated seedlings. Ethylene production in these seedlings peaks at 60 to 96 h, and then declines back to almost wild-type levels. Ethylene overproduction in eto1 and eto3 is limited mainly to etiol ated seedlings; light-grown seedlings and various adult tissues produce clo se to wild-type amounts of ethylene. Several compounds that induce ethylene biosynthesis in wild-type, etiolated seedlings through distinct 1-aminocyc lopropane-1-carboxylic acid (ACC) synthase (ACS) isoforms were found to act synergistically with eto1 and eto3, as did the ethylene-insensitive mutati on etr1 (ethylene resistant), which blocks feedback inhibition of biosynthe sis. ACS activity, the rate-limiting step of ethylene biosynthesis, was hig hly elevated in both eto1 and eto3 mutant seedlings, even though RNA gel-bl ot analysis demonstrated that the steady-state level of ACS mRNA was not in creased, including that of a novel Arabidopsis ACS gene that was identified . Measurements of the conversion of ACC to ethylene by intact seedlings ind icated that the mutations did not affect conjugation of ACC or the activity of ACC oxidase, the final step of ethylene biosynthesis. Taken together, t hese data suggest that the eto1 and eto3 mutations elevate ethylene biosynt hesis by affecting the posttranscriptional regulation of ACS.