vostok
Well-Known Member
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 or trichome number
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, 199
. 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., 199
. 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., 199
. 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”
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.
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 or trichome number
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, 199

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., 199


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”
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.