Jasmine: SAR vs JAR & the need to Defoil. (its deep)

Discussion in 'Advanced Growing Techniques' started by vostok, Jun 27, 2019.

  1. Harpin Proteins. What’s everyone’s thoughts? I’ve tried them, they’re really rather interesting; especially when considering SAR vs Jasmonic response. Most of the response the plant shows after application is through stimulation of the jasmonic response (JAR).
    Some brief notes on Arabidopsis trichome response to jasmonic acid (which stimulates the jasmonic pathways), salicylic acid (for inducing a SAR response, through salicylic response pathways), as well as artificial damage. Interesting to note how stress response can be desired at times, when the correct conditions are met to stimulate the biomechanics of countering said stress.

    “In a series of experiments, we addressed the effects of artificial damage, jasmonic acid, salicylic acid, and gibberellin on induction of trichomes in Arabidopsis. Artificial damage and jasmonic acid caused significant increases in trichome production of leaves. The jar1-1 mutant exhibited normal trichome induction following treatment with jasmonic acid, suggesting that adenylation of jasmonic acid is not necessary. Salicylic acid had a negative effect on trichome production and consistently reduced the effect of jasmonic acid, suggesting negative cross-talk between the jasmonate and salicylate-dependent defense pathways. Interestingly, the effect of salicylic acid persisted in the nim1-1 mutant, suggesting that the Npr1/Nim1 gene is not downstream of salicylic acid in the negative regulation of trichome production. Last, we found that gibberellin and jasmonic acid had a synergistic effect on the induction of trichomes, suggesting important interactions between these two compounds.
    Many plant species respond to insect damage by increasing the density and/or number of trichomes on new leaves (Myers and Bazely, 1991; Agrawal, 1998, 1999, 2000; Traw, 2002; Traw and Dawson, 2002a). This structural barrier is an important component of resistance to herbivores for plants in general (Levin, 1973; Agren and Schemske, 1994; Fernandes, 1994; Traw and Dawson, 2002b) and for the model plant, Arabidopsis, in particular (Mauricio and Rausher, 1997).

    In the current study, we show that two other major plant chemicals, jasmonic acid and salicylic acid, also influence trichome production in Arabidopsis.
    Induction of resistance to herbivores and pathogens is generally regulated by a network of signal transduction pathways in which salicylic acid and jasmonic acid function as key signaling molecules (Glazebrook, 2001; Thomma et al., 2001; Kunkel and Brooks, 2002). Herbivore damage and artificial wounding both cause rapid increases in jasmonic acid (Bostock, 1999; Reymond et al., 2000), triggering systemic defenses against herbivores and necrotrophic pathogens. In contrast, infection by biotrophic pathogens causes rapid increases in salicylic acid (Gaffney et al., 1993; Ryals et al., 1994) and systemic expression of defenses against these pathogens. There is substantial evidence that salicylic acid negatively regulates the jasmonate-dependent pathway in many plants (Bostock et al., 2001; Thaler et al., 2002), including Arabidopsis (Spoel et al., 2003; Traw et al., 2003). Despite clear potential for negative cross-talk with respect to structural plant defenses, to our knowledge, no such pattern has been previously shown.

    Jasmonic Acid Increases Trichome Density and Number
    Artificial wounding and herbivory typically trigger jasmonate-dependent responses in plants (Bostock, 1999; Reymond et al., 2000). Having found that artificial wounding increased trichome production, we predicted that jasmonic acid would also cause up-regulation of trichomes. To test this prediction, we applied 0.6 mL of two concentrations (0.1 and 1 mm) of jasmonic acid or a water control to plants of two lines (Columbia and Wassilewskija) in a completely randomized experiment. For details of treatment application, trichome measurements, and statistical analysis see “Materials and Methods.” We found that jasmonic acid caused significant increases in both trichome density (F1,30 = 16.6, P < 0.001; Fig. 2A) and number (F1,27 = 8.6, P = 0.006; Fig. 2B). There was no difference in the effect of 0.1 and 1 mm jasmonic acid on trichome density (F1,30 = 0.98, P = 0.329; Fig. 2A), but the higher concentration did have a significantly greater effect on trichome number (F1,27 = 5.2, P = 0.029; Fig. 2B). Columbia and Wassilewskija responded similarly to jasmonic acid, as shown by the lack of a significant line by treatment interaction term in the analysis of variance for trichome density (Fig. 2A) or trichome number (Fig. 2B)

    Adenylation of Jasmonic Acid Is Not Required
    The jasmonic acid response mutant (jar1-1) produces jasmonic acid but does not adenylate it (Staswick et al., 2002) and therefore lacks induction of some jasmonate-mediated anti-fungal resistance traits (Staswick et al., 1992, 1998). If the Jar1-1 gene is required for jasmonate-dependent induction of trichomes, then we expected that the jar1-1 mutant would not induce trichomes following the application of jasmonic acid, whereas its wild-type background, Columbia, would. To test this prediction, we treated plants of the jar1-1 mutant and Columbia with 0.6 mL of 0.45 mm jasmonic acid or a water control in a completely randomized experiment. We chose 0.45 mm because it was intermediate between the two concentrations we had previously tested on Columbia. Jasmonic acid caused an increase in trichome density of 55.9% for the jar1-1 mutant and an increase of 52.7% for Columbia. Trichome number increased by 27.1% for the jar1-1 mutant and 34.6% for Columbia. In a two-way analysis of variance, these effects of jasmonic acid were significant for both trichome density (F1,11 = 16.9, P = 0.001) and trichome number (F1,11 = 7.4, P = 0.021). The lack of difference in the response of the jar1-1 mutant and its background was shown by the absence of a significant line by treatment effect for either trichome density (F1,11 = 0.01, P = 0.939) or trichome number (F1,11 = 0.39, P = 0.545). This result suggests that the Jar1-1 gene is not required for the induction of trichomes.

    Salicylic Acid Decreases Trichome Density and Number
    Given that the jasmonate and salicylate pathways generally exhibit negative cross-talk in Arabidopsis (Spoel et al., 2003; Traw et al., 2003; but see van Poecke and Dicke, 2002), we predicted that exogenous salicylic acid would reduce trichome density and number. To test this prediction, we applied two concentrations (0.1 and 1 mm) of salicylic acid or a water control to plants of two lines (Columbia and Wassilewskija) in a completely randomized experiment. We found that salicylic acid caused significant decreases in both trichome density (F1,33 = 7.9, P = 0.008; Fig. 3A) and number (F1,33 = 4.6, P = 0.039; Fig. 3B). There was no difference in the effect of 0.1 and 1 mm salicylic acid on trichome density (F1,33 = 2.6, P = 0.115; Fig. 3A) or trichome number (F1,33 = 3.3, P = 0.076; Fig. 3B). Columbia and Wassilewskija responded similarly to salicylic acid, as shown by the lack of a significant line by treatment interaction term in the analysis of variance for trichome density (Fig. 3A) or trichome number (Fig. 3B). We repeated the experiment with similar results.

    Gibberellin and Jasmonic Acid Have a Synergistic Effect on Trichome Induction
    Gibberellin is a hormone that regulates plant growth and developmental events ranging from seed germination to the timing of flowering and senescence. Gibberellin appears to have a primary role in initiating Arabidopsis trichomes (Chien and Sussex, 1996; Telfer et al., 1997; Perazza et al., 1998). For example, the ga1-3 mutant is unable to produce gibberellin and does not produce trichomes. However, when gibberellin is added exogenously, trichome production is restored (Chien and Sussex, 1996). Additionally, wild-type plants are unable to produce trichomes following treatment with two gibberellin biosynthesis inhibitors, paclobutrazol (Chien and Sussex, 1996) and uniconazole (Perazza et al., 1998). Given our observation of positive effects of jasmonic acid on trichome production, we initiated study of how jasmonic acid and salicylic acid interact with gibberellin in the production of trichomes.

    To address the interactions among jasmonic acid, salicylic acid, and gibberellin, we applied a 0.45 mm concentration of each compound alone and in all possible combinations. We applied these treatments to plants of Landsberg erecta in a completely randomized experiment. We chose Landsberg erecta because this is the wild-type background for important gibberellin mutants. For details of treatment application, trichome measurements, and statistical analysis, see “Materials and Methods.”
    There were strong interactions between jasmonic acid and gibberellin (Table II). In the absence of gibberellin, leaves of plants treated with jasmonic acid exhibited an increase of only 5% in trichome density and number. In the presence of gibberellin, leaves of plants treated with jasmonic acid increased 48.9% in trichome density and 93.1% in trichome number. The greater effect of jasmonic acid in the presence of gibberellin was significant according to the jasmonic acid by gibberellin interaction term in the analysis of variance for trichome density”
    From the following journal

    This journal was really thorough, and brings up many of things to be considered when looking at the overall image of plant health vs what qualities we desire from it. If we’re looking for the highest production of trichome, it increasingly seems that some of this additional production is stimulated from stress / artificial damage response. Also makes me wonder how we achieve the most optimal balance using products like aloe powder with raises the SAR and harpin proteins raising JAR.

    “One of the most remarkable features of trichomes is their capacity to synthesize, store and sometimes secrete large amounts and varied types of specialized metabolites (see Figure 2 for examples). These include various classes of terpenes (Gershenzon et al., 1992; Hallahan, 2000; van der Hoeven et al., 2000), as well as phenylpropanoid derivatives (Gang et al., 2001), acyl sugars (Kroumova and Wagner, 2003; Li and Steffens, 2000), methylketones (Fridman et al., 2005) and flavonoids (Voirin et al., 1993). Many trichome-borne compounds have significant commercial value as pharmaceuticals, fragrances, food additives and natural pesticides (Duke et al., 2000; Wagner, 1991; Wagner et al., 2004). For this reason, the prospect of exploiting trichomes as ‘chemical factories’ to produce high-value plant products has recently caught the attention of plant biochemists and biotechnologists alike (Duke et al., 2000; Mahmoud and Croteau, 2002; Wagner et al., 2004). Because they are epidermal appendages, the contents of trichomes can be sampled relatively easily, facilitating analysis of small molecules, proteins and mRNAs (Fridman et al., 2005; Gang et al., 2001; Gershenzon et al., 1992). This has permitted the identification of biosynthetic enzymes for a variety of pathways.
    When considering the biosynthetic pathways for the specialized metabolites in trichomes, it is important to note that, in most cases, trichomes are not connected to the vascular system of the plant and instead are appendages extending from the epidermis. Moreover, the glandular parts of the trichomes are generally not strongly photosynthetic: many are pale green or completely non-green, and data mining of glandular trichome EST databases has indicated low levels of expression at best for genes encoding the components of the photosynthetic apparatus or enzymes of many basic biochemical pathways (e.g. Fridman et al., 2005; Lange et al., 2000). Analyses of such EST databases have further shown that the trichomes operate as a closed biochemical system with a simple input and few highly active biochemical pathways of both primary metabolism (for generating energy and precursors) and specialized metabolism (for generating final products; Gang et al., 2001). The primary metabolite that fulfils a dual role as the energy source and the starting material for building blocks is probably sucrose in most cases, as it can easily be imported into the trichome.
    Terpenes constitute a coherent class of compounds that are all biosynthetically derived from the same basic C5 building blocks [isopentenyl diphosphate (IPP) and dimethylallyl diphosphate (DMAPP)]. In addition to multiple isomers of the simple mono- (C10), sesqui- (C15) and di- (C20) terpenes, the terpene backbones are often further modified by oxidation reactions and conjugation to other moieties, and consequently the total number of plant-synthesized terpenes is estimated in the tens of thousands (see Figure 2 for examples). Terpenes are widespread in the plant kingdom and beyond, and therefore it is not surprising that the biochemical pathways leading to their biosynthesis have been highly studied. They are also present in the trichomes of many plants. The pioneering work of Croteau et al. (2005) on the biochemical pathway for synthesis of menthol via limonene in mint (Mentha piperita, Lamiaceae) peltate glands, using classical enzyme purification and EST database mining, resulted in identification of most of the enzymes of this pathway, including the heterodimeric geranyl diphosphate synthase (GPPS, an enzyme that uses IPP and DMAPP), the monoterpene synthase limonene cyclase, and additional modifying enzymes including cytochrome P450 mono-oxygenases and dehydrogenases (Croteau et al., 2005).

    Solanaceae trichomes are also known to express terpene synthases and produce a variety of terpenes (Guo and Wagner, 1995). In tobacco, the diterpenes cembratrieneols (CBTols) and cembratrienediols (CBTdiols), important defense compounds, are produced in the trichomes (Wang and Wagner, 2003; Wang et al., 2001). CBTols are first synthesized from geranylgeranyl diphosphate (GGPP) in a reaction catalyzed by a diterpene synthase, and can then be modified to the CBTdiols in an oxidation reaction catalyzed by a cytochrome P450 enzyme. The genes encoding these two enzymes have been shown to be expressed in the trichomes (Wang et al., 2001), and, at least in the case of the cytochrome P450, specifically in the cell at the tip of a long trichome (Wang et al., 2002). Presumably, the entire terpene pathway is active in this cell. Tomato species are also known to produce various terpenes in their glands. Li et al. (2004) and van Schie et al. (2007) showed that expression of the monoterpene-forming enzyme linalool synthase, which also occurs mostly in the glands, could be induced by treating the plant with methyl jasmonate.
    The trichomes of Artemisia annua (Asteraceae) produce the compound artemisinin, which has recently received renewed attention as a drug to treat malaria (Chang et al., 2007). Artemisinin is a sesquiterpene with five oxygens, including a peroxide group (Chang et al., 2007). The sesquiterpene backbone is synthesized from the precursor farnesyl diphosphate (FPP) by the enzyme amorpha-4,11-diene synthase (Mercke et al., 2000), and one of the enzymes responsible for the subsequent oxidation reactions has been identified (Teoh et al., 2006), although none of the enzymes responsible for the downstream steps are known.

    Phenylpropanoids, polyketides and mixed-type compounds
    Phenylpropanoids are also commonly found in trichomes. For example, in some varieties of basil, the peltate glands not only make terpenes but also phenylpropanoids, mostly the phenylpropenes chavicol, eugenol, methylchavicol and methyleugenol (Gang et al., 2001). These compounds are synthesized from monolignol alcohol precursors in a pathway that involves acetylation, reduction and methylation (Gang et al., 2002; Koeduka et al., 2006). Trichomes of Phyllyrea latifolia (Oleaceae) accumulate flavonoid glycosides (Tattini and Gucci, 1999), and those of Orobanche ramose (Orobanchaceae) accumulate both (unspecified) phenylpropanoids and monoterpenes (Sacchetti et al., 2003). Flavonoid aglycones are found on the surface of many plant species (Wollenweber, 1984), and are found in the peltate glands of peppermint (Mentha × piperita) leaves (Voirin et al., 1993), apparently dissolved in the hydrophobic terpene matrix.
    Other polyketides in addition to flavonoids are also found in the trichomes. Primin, a benzoquinone that causes dermatitis, is synthesized by a polyketide synthase in the trichomes of Primula obconica (Primulaceae) from hexanoyl CoA and three malonyl CoA units, giving the intermediate olivetolic acid, followed by decarboxylation, hydroxylation and methylation (Horper and Marner, 1996). In the family Cannabaceae, the trichomes of Cannabis sativa produce and accumulate the psychoactive tetrahydrocannabinol, which is synthesized through C10 prenylation of olivetolic acid, followed by a cyclization reaction and decarboxylation (Raharjo et al., 2004). In hops (Humulus lupulus, Cannabaceae), which provide flavor to beer, the trichomes contain, in addition to terpenes, many C5-prenylated polyketides, with the major compound being xanthohumol (Figure 2; Matousek et al., 2002). Lower levels of more oxidized prenylated polyketides, the so-called ‘bitter acids’ (e.g. humulone), are also present and are important for the flavor (Fung et al., 1997). Analysis of an EST database constructed from hops glands, followed by biochemical assays of candidate enzymes, have recently identified a methyltransferase involved in the synthesis of xanthohumol (Nagel et al., 2008).

    Fatty acid derivatives
    Many specialized metabolites in trichomes are derived from fatty acids or have fatty acid moieties. As described above, the synthesis of olivetolic acid, which is one of the precursors in the synthesis of both priming and tetrahydrocannabinol, requires hexanoic acid as a precursor. The type VI trichomes of Solanum habrochaites glabratum (previously named Lycopersicon hirsutum glabratum) synthesize insecticidal C11, C13 and C15 methylketones by hydrolysis of the ß-ketoacyl ACP intermediates of fatty acid biosynthesis, followed by decarboxylation (Fridman et al., 2005). Both reactions are catalyzed by the same enzyme, methylketone synthase (MKS), which is related to other plant esterases (Fridman et al., 2005). Analysis of a type VI-specific EST database showed that the genes encoding enzymes for fatty acid biosynthesis in the plastids are highly expressed, as is MKS (Fridman et al., 2005).
    In the type IV glands of the related species Solanum pennellii (previously Lycopersicon pennellii), as well as in many other Solanaceae species, including tobacco, Datura and Petunia spp., glucose and sucrose are acylated with 3–4 acyl groups of both straight and branched chains ranging in carbon number from 2 to 12 (Van Dam and Hare, 1998). The resulting polyester acyl sugars (Figure 2) are secreted from the glands, sometimes in relatively large quantities, and the exudate causes the plant surface to become sticky and provides a strong deterrent to insects. The first acylation reaction of glucose is catalyzed by UDP-glucose fatty acid:glycosyltransferase, and additional acylations of the sugar moiety appear to occur by a series of disproportionation reactions, the first of which is catalyzed by an enzyme that belongs to the serine carboxypeptidase family (Li and Steffens, 2000). The subsequent reactions have not been yet characterized. The acyl groups are derived from elongation of short straight and branched fatty acids, which themselves are derived from degradation of amino acids (Walters and Steffens, 1990). It appears that, in Solanum and Datura species, elongation occurs via the fatty acid biosynthetic pathway, thus adding two carbons to the chain per cycle, while in tobacco and petunia, elongation occurs via the a-ketoacid route that also operates in leucine biosynthesis as well as in the synthesis of glucosinolates (Kroumova and Wagner, 2003).
    Ranger et al. (2005) have reported that the stem trichomes of an alfalfa (Medicago sativa, Leguminosae) line that is resistant to potato leafhopper contain a series of N(3-methylbutyl)amides of saturated C14, C15, C16 and C18 fatty acids, and that these compounds may contribute to the observed resistance (see Figure 2 for an example). The enzymes responsible for the synthesis of these amides have not yet been described.
    Interplay among competing pathways
    Because the biosynthetic capacity of the trichomes is limited by the amount and type of the carbon source imported into them, it is not surprising that, even when a given type of trichome is capable of synthesizing different classes of compounds, the total output is limited. For example, the peltate glands of various cultivars of basil synthesize either predominantly terpenes, predominantly phenylpropenes or a mixture of both, and the output of one class of compounds is inversely correlated with the levels of the other (Iijima et al., 2004a). Similarly, the type VI glands of S. habrochaites glabratum synthesize high amounts of methylketones and low amounts of terpenes, while the glands of some other S. habrochaites accessions contain high levels of sesquiterpene acids and no methylketones (Fridman et al., 2005). These differences are controlled at the transcriptional level, although the components of the regulatory mechanism have not yet been identified.”

    “Production of acid-soluble conjugated di- and polyamines, like that of other secondary metabolites, is enhanced by exposure to methyl jasmonate (MJ). We investigated this metabolic response, and activities of enzymes involved in putrescine (Put) and tropane alkaloid biosynthesis, in root cultures of Hyoscyamus muticus and compared it with that of callus cultures. In root cultures, free Put and N-methylputrescine (mPut) increased upon treatment with MJ, whereas in callus cultures mPut levels were not affected. Differently from roots, conjugated amines were scarce or absent in callus cultures, and accumulated only transiently upon treatment with MJ. Arginine decarboxylase, ornithine decarboxylase and diamine oxidase activities in root cultures were strongly stimulated by treatment with MJ, but were inhibited in callus cultures. Exposure to MJ also enhanced putrescine N-methyltransferase activity in root cultures more than in callus cultures. These results are discussed in relation to the different capacity for tropane alkaloid production in the two culture systems”

    Here it does talk about “Exposure to MJ (Methyl Jasmonate) also enhanced putrescine N-methyltransferase activity in root cultures more than in callus cultures.” This is something that seems potential mode of actions in biosynthesis stimulation considering what we know of cannabinoid biosynthesis / production.

    The majority of the organic acids (oxalic acid, shikimic acid, malonic acid, threonic acid, glyceric acid, and galactaric acid) responsive to heat or elevated CO2 found in this study are involved in several metabolic pathways, in particular stress defense pathways. Oxalic acid is known to be involved in antioxidant stress defense (Ding et al., 2007; Jiang et al., 2008; Zhang et al., 2001). Exogenous application of oxalic acid improved heat tolerance of pepper (Capsicum annuum) (Zhang et al., 2001) and alfalfa by enhancing chlorophyll accumulation and increasing antioxidant enzyme activities that was inhibited by heat stress (Jiang et al., 2008). Its accumulation has also been associated with drought tolerance in creeping bentgrass [Agrostis stolonifera (Merewitz et al., 2012)] and cold tolerance in arabidopsis [Arabidopsis thaliana (Korn et al., 2010)]. Shikimic acid is involved in the production of polyphenol flavonoid compounds such as anthocyanins, which have antioxidant properties to suppress heat-induced oxidative damage (Shao et al., 2007). Xu and Huang (2012) reported a decrease in shikimic acid resulting from drought stress in kentucky bluegrass. Little is known about the direct effects of elevated CO2 on shikimic acid, but studies have shown an increase in secondary metabolites derived from the shikimic acid pathway such as tannins in response to enriched CO2 (Lindroth et al., 2001; Peñuelas and Estiarte, 1998). Malonic acid is a dicarboxylic acid and malonate is its ionized form. Malonate acts as a major competitive inhibitor of succinate dehydrogenase involved in the tricarboxylic acid cycle of respiration (Li and Copeland, 2000). Malonate also has been associated with osmotic adjustment and stress defensive system (Lecoeur et al., 1992; Li and Copeland, 2000). Threonic acid is a metabolic product of ascorbic acid and also correlated with glyceric acid synthesis (Helsper and Loewus, 1982). Threonic acid and glyceric acid have been reported to be sensitive to heat stress in many species, including arabidopsis (Kaplan et al., 2004), hybrid bermudagrass, and kentucky bluegrass (Du et al., 2011). Galactaric acid is derived from galacturonic acid by galacturonic acid oxidase, which has been found to stimulate the oxidation of indole acetic acid by peroxidase (Pressey, 1991) and acts as a substrate for galacturonic acid reductase leading to the synthesis of ascorbic acid. Sanchez et al. (2008) reported that galactaric acid was decreased by salinity in arabidopsis. The decline in the abundance of these organic acids under heat stress suggested that heat stress mainly weakened the stress defense mechanisms, whereas the increases or maintenance of the abundance of those organic acids in plants exposed to elevated CO2 under heat stress could contribute to the improvement in heat tolerance by enhancing or maintaining more active oxidative defense mechanisms. However, direct mechanisms of CO2 mitigation of heat damage involving these organic acids are yet to be determined.
    Monosaccharides such as glucose, fructose, and galactose have important functions such as serving as energy sources and osmoregulants, whereas disaccharides such as sucrose and maltose are the main forms of carbohydrates for transport and storage in plants (Kaplan et al., 2004; Merewitz et al., 2012; Urbonaviciute et al., 2006).
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  2. Good read. I'll be putting some of that to experimentation once the perpetual sog is going.

    Should be able to try a bunch of methods and degrees of torture in a short period. Lol
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  3. I've hit my plants with (toomuch?) JA before. Freaked them out hard, stopped growing, yellow leaves FAST, and ... a hella lot more trichomes.
    I've also read in literature that researchers add only smaller amount and spray throughout flower, but I know that you can just hit it hard once and yea... lol
    I'd do it again. Makes the plant think its getting attacked by 1000000000000000000000000000000000000 spider mites all at once.

    Nice post vostok! Imma come back a lil later and read it some more (that kinda long!) and digest the info some more.
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  4. That’s a tough one to read start to finish bud. Very nice info though thanks.

    Sent from my iPhone using Grasscity Forum
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  5. Salicylates are poison, personally. Most cases of tinnitus are from daily mouthwash ingestion. Anyone adding aspirin or Wintergreen to pot has lost their mind. Imo. Any anyone feeding jasmonic acid, why not force the plant to make its own natural Cannabis derived jas?

    That's actually one of multiple reasons Cali weed sucks today. The plant isn't biosynthesizing half of what it should be, namely fatty acids which so many other substances including skunk thiols are derived from. Cannabis was never a plant that protected herself. She protects her offspring. Just to give an idea on how lost the modern understanding of Cannabis is. "Thc and limonene", sorry that ain't gonna cut it, Marlborough man. We need linolenic acid,lots of it. The growers of old werent stupid, they would have grown sensi if it made sense to grow shitty weed with no fatty acids.
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  6. Yeah, we need the Cliffs Notes version.
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  7. short version, try this product out and let us know what happens.
    I will if you buy it for me. Costs $200.
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