More exact ppm values of individual elements
- Thread starter Flowki
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Xs121
Well-Known Member
Interesting
What really caught my eye is how you use your N, in which I tend to agree. In fact, I run my N up to 150ppm, up to 5wks of 12/12, total solute EC up to 1.4. Beyond 5-6wks of 12/12, my N starts dropping off to 50-25ppm, I still run my EC pretty high though from 1 - 1.5, until the wk before the final wk. At which point my EC would be .5 or less.
I use to defoliate heavily but using this kind of feeding by the last 2 weeks of flowering, most if not all my fan leaves have turned yellow or fading without sacrificing buds health.
im4satori
Well-Known Member
ya bro I run my N at half what your feeding
full strength
veg N 117 ppm
early bloom N 85-90ppm
late bloom 75 ppm
if I ran 150ppm of N at any stage it would be way too much
Xs121
Well-Known Member
You run higher than me in late bloom. lol
Otherwise, yes, I like to push my N and PK, but I keep an eye on my plants. As for N, if the leaves start turning really really dark than their normal hue or starts to show a bit of claw, I backed off my N and let them feed on what N they have.
im4satori
Well-Known Member
im4satori
Well-Known Member
looks great
KonopCh
Well-Known Member
How do you calculate those numbers from nutrient bottle?
Mine has 5-4-8 for example and I want to know how I calculate and adjust those numbers.
im4satori
Well-Known Member
start by down loading hydrobuddy
im4satori
Well-Known Member
5-4-8 throws out finished numbers very close the the jacks 321 mix
Dr. Who
Well-Known Member
OK, not coming out and calling things bad or you bad...Not a personal attack ...OK..
You have yellowing way to early...The pics show more then overuse of P...plenty more. Points to one issue - "to me."
I see that pic and I see a period of pH being low and the plant is reacting to block's from the imbalance.... Ca, P and other micro's being blocked..
Now if you come in and reply to me that your pH was never out of range.....1 question for that...What are you holding pH wise? Give me your low set point and how high do you let her rise before adjusting?
OR
Too much P and your plant is reacting to that....
To me it's more likely the first one as you are running a high N and that buffers high P for late bloom...Your NPK numbers are ok, other then the N being a bit high..
Xs121
Well-Known Member
No attack, valid question and good observation.
Ph at feeding 5.6, by next feeding, ph is at 5.9-6.1. Medium is perlite and hydroton
As to yellowing, if you ask me, it's not fast enough. You know me by now that in a sense if I'm still feeding my plants the old way......at this point I would have removed all those fan leaves (you should try defoliation) but I know you like green leaves at late bloom.....I don't. The way I look at it, I'm not growing for healthy leaves up to late bloom...the sooner I can get rid of them the better....my focus is in the bud structure whether you agree with that or not.
As to N or any element for that matter....like I've said in my previous post...I don't follow stage feeding or conventional feeding. Like the way you guys do
seedling - N ppm?
vegetative - N ppm?
early flowering - N ppm?
flowering - N ppm?
late bloom - N ppm?
I don't do that feeding of certain specific ppm for certain stage.
From early vegetative to 5 wks of flowering.. My N 'cycle' from 25ppm to 150 ppm and back to 25 ppm again, repeating the cycle.....at any given time (not plant stages)...it all depends on the condition of the plant....there is no set schedule or plant stage as to when Im feeding them with 150 ppm....I let the plant decide if its ready for 150 ppm... I hope this makes it clear.
It's like wet/dry cycle of watering your plant. If we do that in watering, I do the same with fertilizer.
As to P...what's wrong with high P? Do you know what kind of hormone is affected when P is abundant? Same question with N, what kind of hormone is impacted when N is abundant? Nah, I'm not going there, that's beyond the scope of this topic which is ppm.
I don't fertilize, I manipulate plant hormone.
Regardless, Im not trying to convince anybody that my feeding is the right way, just sharing my way of feeding and I'm very happy with the result and the quality of the buds.
Roger A. Shrubber
Well-Known Member
P Availability Alters Hormone Sensitivity in the Root
To maximize the capability of an organ to expand or elongate, or to establish a particular developmental program such as root branching, plants have evolved mechanisms tightly coupled to the perception of environmental stimuli. Many of the plant responses to environmental factors are mediated by phytohormones, such as auxin and ethylene. To address the question of the role of phytohormones on the morphogenetic changes induced by P availability, we analyzed the effect of auxin, cytokinins, and ethylene on root architecture and lateral root formation at low and high P levels.
Treatment of high P-grown plants with 2,4-D inhibited primary root growth, induced formation of lateral roots and increased lateral root density. Moreover, 10−8 m 2,4-D was sufficient to reproduce the low P response in terms of lateral root density and inhibition of primary root growth (Figs. (Figs.1,1, D and E, and 3, A–C). Treatment of high P-grown plants with cytokinins also had an inhibitory effect on primary root growth, but in contrast to auxins, cytokinins inhibited lateral root formation and resulted in a reduction of lateral root density. These results suggest that under low P conditions, an increase in auxin synthesis and/or alterations in the polar transport of auxins mediate the changes in root system architecture. However, the finding that lateral root density in low P seedlings is affected by concentrations of 2,4-D 2 orders of magnitude lower than those required to have a similar effect on high P seedlings suggests that P-starved plants have a higher sensitivity to auxins (Fig. (Fig.3A).3A). Therefore, changes in the auxin sensitivity of the root seem to be involved in the developmental response of the Arabidopsis root system to P starvation.
Auxin is synthesized in the young leaves of the shoot system and transported downward to the root through the vascular tissues (Casimiro et al., 2001). The formation and maintenance of auxin gradients are thought to occur through the action of a specific polar auxin transport system that requires active efflux of auxin (Estelle, 1998). Recently, polar auxin transport has been shown to be essential for lateral root development (Reed et al., 1998; Casimiro et al., 2001). We used TIBA, an auxin transport inhibitor, to gain knowledge of the participation of auxin transport on lateral root development in response to P availability. Primary root elongation in low P seedlings was more sensitive to TIBA than in high P seedlings (Fig. (Fig.4A);4A); however, P-deprived plants showed lower sensitivity to the negative effect of TIBA on lateral root formation and lateral root density when compared with high P-grown plants (Fig. (Fig.4,4, B and C). Because it is known that auxins inhibit primary root elongation and stimulate lateral root formation, these observations appear somewhat paradoxical. However, it has recently been reported that treatment with auxin transport inhibitors results in suboptimal levels of auxins for lateral root initiation, but also in the accumulation of auxins in the root meristem (Casimiro et al., 2001). An increase in auxin sensitivity could explain why in low P seedlings, suboptimal levels of auxins resulting from TIBA treatment are sufficient to maintain lateral root formation. Moreover, increased auxin sensitivity together with an increased level of auxins in the root meristem could explain the enhanced TIBA inhibition of primary root elongation in low P seedlings.
Using the developmental changes that occur in the Arabidopsis root in response to high and low P, we have isolated Arabidopsis mutants that are unable to respond to P deprivation in terms of lateral root formation and inhibition of primary root elongation (J. López-Bucio, E. Hernández-Abreu, and L. Herrera-Estrella, unpublished data). Some of these mutants are partially auxin resistant at low P, but not at high P. These results also support the notion that the developmental response of the Arabidopsis root system to low P availability involves changes in auxin sensitivity.
Recently, it has been demonstrated that auxin also moves basipetally, from the root apex to the root-shoot junction (Rashotte et al., 2000). To date, it is not clear which of these auxin transport systems actually control lateral root formation (Casimiro et al., 2001). The use of TIBA demonstrates that auxin transport is required for roots to correctly respond to P availability. The close proximity of lateral roots to the root apex of plants grown under low P opens the possibility that basipetal transport of auxin could be involved in controlling the proliferation of lateral roots in response to P deficiency (Fig. (Fig.1B).1B). However, because shoot apical synthesis of auxins is a large source of root auxins, an important role for acropetal transport of auxin cannot be excluded.
from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC155888/
Regulation of CK biosynthesis by nitrogen
Until the identification of genes encoding adenosine phosphate-isopentenyltransferase (IPT), which catalyses the initial step of CK biosynthesis, it was believed that CKs are synthesized in roots (Letham, 1994). In Arabidopsis, IPT is encoded by seven genes that are differentially expressed in various tissues, indicating that CK production is not confined to roots (Miyawaki et al., 2004; Takei et al., 2004). Among these seven genes, AtIPT3 is nitrate inducible. Accumulation of CKs was greatly attenuated in an atipt3 mutant, indicating that AtIPT3 is a key determinant of nitrate-dependent CK biosynthesis (Miyawaki et al., 2004; Takei et al., 2004). Interestingly, nitrate-inducible expression of AtIPT3 was also observed in detached shoots (Miyawaki et al., 2004). Similarly, nitrogen supplementation induces CK accumulation in detached sunflower and tobacco leaves (Salama and Wareing, 1979; Singh et al., 1992). Microarray analyses have shown that the nitrate-inducible expression of AtIPT3 is partly mediated by NRT1.1/CHL1 (NRT1.1), a protein which functions as a dual-affinity nitrate transporter and nitrate sensor (Liu et al., 1999; Ho et al., 2009; Wang et al., 2009). AtIPT3 is expressed in phloem throughout the plant (Miyawaki et al., 2004; Takei et al., 2004), and this expression pattern overlaps with that of NRT1.1 in roots (Guo et al., 2001). However, in shoots, NRT1.1 expression is detected only in young leaves (Guo et al., 2001). Therefore, whether or not NRT1.1 mediates nitrate-inducible AtIPT3 expression in shoots is an open question. Given that AtIPT3 is expressed in phloem, it is likely that CKs synthesized by AtIPT3 in shoots function as a shoot-to-root long-distance signal of shoot nitrate availability. In this context, it has been shown that xylem sap predominantly contains trans-zeatin (tZ)-type CKs, and phloem sap mostly contains N6-(Δ2-isopentenyl)adenine (iP)-type and cis-zeatin (cZ)-type CKs (Hirose et al., 200
. Thus, either the iP- or cZ-type CKs, or possibly both, could be the shoot-to-root long-distance signal in Arabidopsis. Grafting experiments using a higher order atipt mutant (atipt1;3;5;7) have provided unequivocal evidence that iP-type CKs are translocated from the shoot to the root (Matsumoto-Kitano et al., 200. The atipt1;3;5;7 mutant is characterized by extremely low iP- and tZ-type cytokinin levels, retarded shoot growth, and enhanced lateral root outgrowth. When a wild-type shoot was grafted onto the atipt1;3;5;7 mutant root, the normal growth phenotype and levels of iP-type CKs were restored in the mutant root, indicating that iP-type CKs translocated from the shoot are biologically functional (Matsumoto-Kitano et al., 200. Notably, the expression of AtIPT3 is also regulated by iron, phosphate, and sulphate availability, both in shoots and in roots (Hirose et al., 2008; Seguela et al., 200. It could be that AtIPT3 functions as an integrator of nutrient availability signals.from https://academic.oup.com/jxb/article/62/4/1399/464311
i don't understand but about half of this, and it's taken me three years of reading and studying to get half way...
Xs121
Well-Known Member
Good research. Now the question is, how do you apply that to growing cannabis? There are lots of research out there that pertain to fertilizer and hormone. IMO, the only way to find out the effect of the individual element is to push it. If its good (according to my opinion of course) keep doing it. Again, this is just my own personal observation based on my own grows.P Availability Alters Hormone Sensitivity in the Root
To maximize the capability of an organ to expand or elongate, or to establish a particular developmental program such as root branching, plants have evolved mechanisms tightly coupled to the perception of environmental stimuli. Many of the plant responses to environmental factors are mediated by phytohormones, such as auxin and ethylene. To address the question of the role of phytohormones on the morphogenetic changes induced by P availability, we analyzed the effect of auxin, cytokinins, and ethylene on root architecture and lateral root formation at low and high P levels.
Treatment of high P-grown plants with 2,4-D inhibited primary root growth, induced formation of lateral roots and increased lateral root density. Moreover, 10−8 m 2,4-D was sufficient to reproduce the low P response in terms of lateral root density and inhibition of primary root growth (Figs. (Figs.1,1, D and E, and 3, A–C). Treatment of high P-grown plants with cytokinins also had an inhibitory effect on primary root growth, but in contrast to auxins, cytokinins inhibited lateral root formation and resulted in a reduction of lateral root density. These results suggest that under low P conditions, an increase in auxin synthesis and/or alterations in the polar transport of auxins mediate the changes in root system architecture. However, the finding that lateral root density in low P seedlings is affected by concentrations of 2,4-D 2 orders of magnitude lower than those required to have a similar effect on high P seedlings suggests that P-starved plants have a higher sensitivity to auxins (Fig. (Fig.3A).3A). Therefore, changes in the auxin sensitivity of the root seem to be involved in the developmental response of the Arabidopsis root system to P starvation.
Auxin is synthesized in the young leaves of the shoot system and transported downward to the root through the vascular tissues (Casimiro et al., 2001). The formation and maintenance of auxin gradients are thought to occur through the action of a specific polar auxin transport system that requires active efflux of auxin (Estelle, 1998). Recently, polar auxin transport has been shown to be essential for lateral root development (Reed et al., 1998; Casimiro et al., 2001). We used TIBA, an auxin transport inhibitor, to gain knowledge of the participation of auxin transport on lateral root development in response to P availability. Primary root elongation in low P seedlings was more sensitive to TIBA than in high P seedlings (Fig. (Fig.4A);4A); however, P-deprived plants showed lower sensitivity to the negative effect of TIBA on lateral root formation and lateral root density when compared with high P-grown plants (Fig. (Fig.4,4, B and C). Because it is known that auxins inhibit primary root elongation and stimulate lateral root formation, these observations appear somewhat paradoxical. However, it has recently been reported that treatment with auxin transport inhibitors results in suboptimal levels of auxins for lateral root initiation, but also in the accumulation of auxins in the root meristem (Casimiro et al., 2001). An increase in auxin sensitivity could explain why in low P seedlings, suboptimal levels of auxins resulting from TIBA treatment are sufficient to maintain lateral root formation. Moreover, increased auxin sensitivity together with an increased level of auxins in the root meristem could explain the enhanced TIBA inhibition of primary root elongation in low P seedlings.
Using the developmental changes that occur in the Arabidopsis root in response to high and low P, we have isolated Arabidopsis mutants that are unable to respond to P deprivation in terms of lateral root formation and inhibition of primary root elongation (J. López-Bucio, E. Hernández-Abreu, and L. Herrera-Estrella, unpublished data). Some of these mutants are partially auxin resistant at low P, but not at high P. These results also support the notion that the developmental response of the Arabidopsis root system to low P availability involves changes in auxin sensitivity.
Recently, it has been demonstrated that auxin also moves basipetally, from the root apex to the root-shoot junction (Rashotte et al., 2000). To date, it is not clear which of these auxin transport systems actually control lateral root formation (Casimiro et al., 2001). The use of TIBA demonstrates that auxin transport is required for roots to correctly respond to P availability. The close proximity of lateral roots to the root apex of plants grown under low P opens the possibility that basipetal transport of auxin could be involved in controlling the proliferation of lateral roots in response to P deficiency (Fig. (Fig.1B).1B). However, because shoot apical synthesis of auxins is a large source of root auxins, an important role for acropetal transport of auxin cannot be excluded.
from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC155888/
Regulation of CK biosynthesis by nitrogen
Until the identification of genes encoding adenosine phosphate-isopentenyltransferase (IPT), which catalyses the initial step of CK biosynthesis, it was believed that CKs are synthesized in roots (Letham, 1994). In Arabidopsis, IPT is encoded by seven genes that are differentially expressed in various tissues, indicating that CK production is not confined to roots (Miyawaki et al., 2004; Takei et al., 2004). Among these seven genes, AtIPT3 is nitrate inducible. Accumulation of CKs was greatly attenuated in an atipt3 mutant, indicating that AtIPT3 is a key determinant of nitrate-dependent CK biosynthesis (Miyawaki et al., 2004; Takei et al., 2004). Interestingly, nitrate-inducible expression of AtIPT3 was also observed in detached shoots (Miyawaki et al., 2004). Similarly, nitrogen supplementation induces CK accumulation in detached sunflower and tobacco leaves (Salama and Wareing, 1979; Singh et al., 1992). Microarray analyses have shown that the nitrate-inducible expression of AtIPT3 is partly mediated by NRT1.1/CHL1 (NRT1.1), a protein which functions as a dual-affinity nitrate transporter and nitrate sensor (Liu et al., 1999; Ho et al., 2009; Wang et al., 2009). AtIPT3 is expressed in phloem throughout the plant (Miyawaki et al., 2004; Takei et al., 2004), and this expression pattern overlaps with that of NRT1.1 in roots (Guo et al., 2001). However, in shoots, NRT1.1 expression is detected only in young leaves (Guo et al., 2001). Therefore, whether or not NRT1.1 mediates nitrate-inducible AtIPT3 expression in shoots is an open question. Given that AtIPT3 is expressed in phloem, it is likely that CKs synthesized by AtIPT3 in shoots function as a shoot-to-root long-distance signal of shoot nitrate availability. In this context, it has been shown that xylem sap predominantly contains trans-zeatin (tZ)-type CKs, and phloem sap mostly contains N6-(Δ2-isopentenyl)adenine (iP)-type and cis-zeatin (cZ)-type CKs (Hirose et al., 200
from https://academic.oup.com/jxb/article/62/4/1399/464311
i don't understand but about half of this, and it's taken me three years of reading and studying to get half way...
Dr. Who
Well-Known Member
NICE POSTING ROGER..P Availability Alters Hormone Sensitivity in the Root
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC155888/
Regulation of CK biosynthesis by nitrogen
Until the identification of genes encoding adenosine phosphate-isopentenyltransferase (IPT), which catalyses the initial step of CK biosynthesis, it was believed that CKs are synthesized in roots (Letham, 1994). In Arabidopsis, IPT is encoded by seven genes that are differentially expressed in various tissues, indicating that CK production is not confined to roots (Miyawaki et al., 2004; Takei et al., 2004). Among these seven genes, AtIPT3 is nitrate inducible. Accumulation of CKs was greatly attenuated in an atipt3 mutant, indicating that AtIPT3 is a key determinant of nitrate-dependent CK biosynthesis (Miyawaki et al., 2004; Takei et al., 2004). Interestingly, nitrate-inducible expression of AtIPT3 was also observed in detached shoots (Miyawaki et al., 2004). Similarly, nitrogen supplementation induces CK accumulation in detached sunflower and tobacco leaves (Salama and Wareing, 1979; Singh et al., 1992). Microarray analyses have shown that the nitrate-inducible expression of AtIPT3 is partly mediated by NRT1.1/CHL1 (NRT1.1), a protein which functions as a dual-affinity nitrate transporter and nitrate sensor (Liu et al., 1999; Ho et al., 2009; Wang et al., 2009). AtIPT3 is expressed in phloem throughout the plant (Miyawaki et al., 2004; Takei et al., 2004), and this expression pattern overlaps with that of NRT1.1 in roots (Guo et al., 2001). However, in shoots, NRT1.1 expression is detected only in young leaves (Guo et al., 2001). Therefore, whether or not NRT1.1 mediates nitrate-inducible AtIPT3 expression in shoots is an open question. Given that AtIPT3 is expressed in phloem, it is likely that CKs synthesized by AtIPT3 in shoots function as a shoot-to-root long-distance signal of shoot nitrate availability. In this context, it has been shown that xylem sap predominantly contains trans-zeatin (tZ)-type CKs, and phloem sap mostly contains N6-(Δ2-isopentenyl)adenine (iP)-type and cis-zeatin (cZ)-type CKs (Hirose et al., 200
from https://academic.oup.com/jxb/article/62/4/1399/464311
i don't understand but about half of this, and it's taken me three years of reading and studying to get half way...
I understand your point and direction (and respect it) but,
I grow for potentials...period!
That's why I asked and observed.
That form of yellowing and necrosis, limited the potential of that plant.......That's my way of growing and grow thinking....
Generally I use very little nutrient in veg at all (in synthetic growing) as I don't use a weak veg soil....My recharged veg soils last about 6 - 8 weeks with need for very little to no feeding (as long as you up pot "on" time.).
In bloom they are getting feed and I don't really change any N level at any "time". I do stop feeding that last week or two. The retained nutrient in the soil. Carry's me out...
Each strain is feed as "it" tells me it needs to be feed (On an NPK value per feeding level).......So simply put, I dial in each strain to the concentrations it likes.
Nice reply,
This is not to be thought of as a defensive or offensive tack. Just a reply..
Dr. Who
Well-Known Member
Well said....I agree..
Flowki
Well-Known Member
Sorry for the late reply, a lot of very good info and I FINALLY understand the differences between the ppm's. Thnx, very appreciated.
EC is what you prefer to use but, how do you convert the ''elemental ppm'' into EC?. This is what I really need to know so that I can somewhat translate other peoples ppm back to the elemental ppm that I am using.
And lastly, any other opinions or more specifics on amount and when?, using ''elemental ppm'' would be preferred if possible. Remember it's only ball park figures that could be applied to all but the most finicky strains.
So far:
EC is what you prefer to use but, how do you convert the ''elemental ppm'' into EC?. This is what I really need to know so that I can somewhat translate other peoples ppm back to the elemental ppm that I am using.
And lastly, any other opinions or more specifics on amount and when?, using ''elemental ppm'' would be preferred if possible. Remember it's only ball park figures that could be applied to all but the most finicky strains.
So far:
Where this is helpful for potential upper/lower values it is vague in stages.
Last edited:
im4satori
Well-Known Member
I recommend you read it again
in response to your post above
I think your still not exactly sure what elemental ppm is
you don't convert the elemental ppm into EC!!!! EC measure electrical conductivity in the solution...
the more mineral in the solution the higher the EC
you can convert EC into the fictitious "ppm" that your ppm meter will provide
for example
EC1.0 = 500ppm (if your meter is on the 5 scale) or 700ppm (if your on the 7 scale)
another words
EC x (either 5 or 7 depending on your meter brand) = fictitious ppm
"elemental ppm" is an individual break down of how much actual ppm (real ppm not fake) of each mineral or nutrient in the finished solution
for example
N 100PPM
P 50 ppm
K 150 ppm
these elemental ppm numbers can be pre determined using a calculator like hydrobuddy
(or if your a smart guy you could do your own math... im not a smart guy so I use the calculator )
definition;
elemental ppm = individual break down for each element in solution
EC = electrical conductivity of said solution
PPM (from a meter) = a fictitious number thru converting EC at a scale of 5/7 that serves no purpose except to confuse people