Lacinilene C

RNAi construct of a cytochrome P450 gene CYP82D109 blocks an early step in the biosynthesis of hemigossypolone and gossypol in transgenic cotton plants.[Pubmed:25794893]

Phytochemistry. 2015 Jul;115:59-69.

Naturally occurring terpenoid aldehydes from cotton, such as hemigossypol, gossypol, hemigossypolone, and the heliocides, are important components of disease and herbivory resistance in cotton. These terpenoids are predominantly found in the glands. Differential screening identified a cytochrome P450 cDNA clone (CYP82D109) from a Gossypium hirsutum cultivar that hybridized to mRNA from glanded cotton but not glandless cotton. Both the D genome cotton Gossypium raimondii and A genome cotton Gossypium arboreum possessed three additional paralogs of the gene. G. hirsutum was transformed with a RNAi construct specific to this gene family and eight transgenic plants were generated stemming from at least five independent transformation events. HPLC analysis showed that RNAi plants, when compared to wild-type Coker 312 (WT) plants, had a 90% reduction in hemigossypolone and heliocides levels, and a 70% reduction in gossypol levels in the terminal leaves, respectively. Analysis of volatile terpenes by GC-MS established presence of an additional terpene (MW: 218) from the RNAi leaf extracts. The (1)H and (13)C NMR spectroscopic analyses showed this compound was delta-cadinen-2-one. Double bond rearrangement of this compound gives 7-hydroxycalamenene, a Lacinilene C pathway intermediate. delta-Cadinen-2-one could be derived from delta-cadinene via a yet to be identified intermediate, delta-cadinen-2-ol. The RNAi construct of CYP82D109 blocks the synthesis of desoxyhemigossypol and increases the induction of Lacinilene C pathway, showing that these pathways are interconnected. Lacinilene C precursors are not constitutively expressed in cotton leaves, and blocking the gossypol pathway by the RNAi construct resulted in a greater induction of the Lacinilene C pathway compounds when challenged by pathogens.

Lacinilene C methyl ether (LCME) constricts tracheal smooth muscle.[Pubmed:3338430]

Environ Res. 1988 Feb;45(1):118-26.

Lacinilene C methyl ether (LCME) is a constituent of the cotton plant and has been implicated as a causative agent of byssinosis. The effect of synthetic LCME on the behavior of isolated strips of canine tracheal smooth muscle (TSM) was examined in tissue bath experiments. LCME (0.64-6.6 x 10(-4) M) caused slowly developing but strong and sustained contractions of TSM strips. Blockade of acetycholine, 5-hydroxytryptamine (5-HT), and histamine H1 receptors with atropine, methysergide, and pyrilamine, respectively, had no effect on constrictions induced by LCME. In contrast, the calcium channel antagonist, verapamil, significantly reduced the response to LCME. Moreover, addition of the beta receptor agonist, isoproterenol, at the peak of LCME-induced contractions relaxed tissues in a concentration-dependent manner. We conclude that LCME elicits contraction of TSM by enhancing the movement of calcium through potential-dependent channels of smooth muscle cell membranes. This mechanism of action does not require activation of specific membrane receptors for acetylcholine, 5-HT, and histamine.