Ethrel-stimulated prolongation of latex flow in the rubber tree (Hevea brasiliensisMuell. Arg.): an Hev b 7-like protein acts as a universal antagonist of rubber particle aggregating factors from lutoids and C-serum

Abstract

Ethrel-stimulated prolongation of latex flow in the rubber tree (Hevea brasiliensis Muell. Arg.): an Hev b 7-like protein acts as a universal antagonist of rubber particle aggregating factors from lutoids and C-serum

Highlights on Hevea brasiliensis (pro)hevein proteins

“…It was also shown that a 44 kDa C-serum protein could inhibit rubber particle aggregation caused by hevein [29]. This Hev b 7-like protein with an anti-aggregation effect is likely to be the antagonist factor previously identified in the C-serum as CS-HLLBP [27], and may also be related to the rubber synthesis inhibitor (m/s 43,700 Da) previously identified by Faridah Yusof et al in 1998 [123].…”

“…The rubber particle aggregation (RPA) inducing effect of hevein has more recently been confirmed [15,29]. It was also shown that a 44 kDa C-serum protein could inhibit rubber particle aggregation caused by hevein [29].…”

“…Citrate accumulated in lutoids may contribute to pH decreases after bursting [23,115]. In addition, mixing lutoid fractions (washed membranes, protein solutions, or debris) with rubber particles leads to coagulation or flocculation [15,28,29]. Indeed, destabilized lutoids react more readily with smaller rubber particles than with large ones [116].…”

“…They possess a single unit membrane (about 80 Ǻ) [24], with a high phosphatidic acid content, in which unsaturated and saturated fatty acids are present in equal proportions [24,25]. Lutoids represent approximately 12% of overall latex [18,19], and help to maintain ion and pH homeostasis [15,18] and control latex coagulation [15,[26][27][28][29]. Lutoid proteins are involved in various biological processes: defense responses, signal transduction, carbohydrate metabolism, chitin catabolism, and proton transport [15].…”

“…Chitinases may also contribute to latex stabilisation by deglycosylating the glycoprotein receptor and abolishing its interaction with hevein. Adapted from[26,29].…”