EVIDENCE FOR AN ELONGATION REDUCTION/C1-ELIMINATION PATHWAY IN THE BIOSYNTHESIS OF N-HEPTANE IN XYLEM OF JEFFREY PINE/

The biosynthetic pathway to n-heptane was investigated by examining th e effect of the beta-keto acyl-acyl carrier protein synthase inhibitor (2R,3S)-2,3-epoxy-4-oxo-7E,10E-dodecadienamide (cerulenin), a thiol r eagent (beta-mercaptoethanol), and an aldehyde-trapping reagent (hydro xylamine) on the biosynthesis of n-[C-14]heptane and putative intermed iates in xylem sections of Jeffrey pine (Pinus jeffreyi Grev. & Balf.) incubated with [C-14]acetate. Cerulenin inhibited C-18 fatty acid bio synthesis but had relatively little effect on radiolabel incorporation into C-8 fatty acyl groups and n-heptane. beta-Mercaptoethanol inhibi ted n-heptane biosynthesis, with a corresponding accumulation of radio label into both octanal and 1-octanol, whereas hydroxylamine inhibited both n-heptane and 1-octanol biosynthesis, with radiolabel accumulati on in octyl oximes. [C-14]Octanal was converted to both n-heptane and l-octanol when incubated with xylem sections, whereas [C-14]1-octanol was converted to octanal and n-heptane in a hydroxylamine-sensitive re action. These results suggest a pathway for the biosynthesis of n-hept ane whereby acetate is polymerized via a typical fatty acid synthase r eaction sequence to yield a C-8 thioester, which subsequently undergoe s a two-electron reduction to generate a free thiol and octanal, the l atter of which alternately undergoes an additional, reversible reducti on to form l-octanol or loss of C1 to generate n-heptane.