Basic genetics explained

[Only Ornamental]

The Breeder knows what he wants Its not really about what others want in my opinion

Shouldn't a good breeder know exactly what his target group wants? Well, in the beginning he should 'choose' his clientele wisely in such that it matches his offerings cause getting chosen is quite risky (what if nobody wants his merchandise?) or alternatively, he could buy some TV commercials to make people love his stuff.
I'm not even sure that too many breeders know more than what they want; which is increasing sales volume, and not 'good', 'fair', or 'innovative' breeding.

 

[Infinitesimal]

first let me say, I don't think of pollen chucker as an inherently derogatory term... depending on context... as pollen chucking is a part of the breeding process. But for a breeder it is just the beginning of a project, as for a chucker it IS the project.

Hmm...
Infinity, maybe he's right but not the way you think . See, several (many?) who name themselves breeders don't feel much about lab and progeny testing. That's why they make S1's thinking all's well trallalla and how practical (thank you marketing!) the buyers think the same too LoL.

Hey OO,

I stand by my statement... regarding his comments, I DO think chemotype breeding is going to be the focus in the future but that wasnt where I was coming from however. I was commenting on the "how" it will be done, which simple pollen chucking will not be the answer... other than through the proverbial needle in the haystack or through genetic bottlenecks which is what we nearly have now in the marketplace. But alas, I don't expect consumers to know about production. As rubbing stems, tells you jack shit about a chemotype . and that seems to be the standard for pollen chucker selection

I agree and that is just it, though... those that don't use progeny testing at least, if not in conjunction with full spectrum chemotype analysis, have a hard time convincing me that they know what they are doing... instead of just chucking pollen and hoping for the best... and are therefore actually "breeders" and not just boasting themselves to be such.

Besides, chemotype testing is not strictly difficult; smoke a joint and you'd know if its THC or CBD (more or less... CBD could also be low THC) or smell the bud and know the flavour. But again, the trick is often not the 'what' but the 'how much' and for that you'll need some sort of test.

this is where, on some level, I will disagree with you... yes progress can be made e.g. DJ short, just going by your own perceptions and feelings... but he also employs progeny testing .

maybe I am wrong but to me, knowing the chemical phenotype encompasses three distinct laboratory measurements.
1) the variety of chemicals found in a specific phenotypic expression
2) the composition/ratio of the various secondary metabolites found within a specific individual's essential oils.
3) the total quantity of secondary metabolite production found within a specific individual.

now since your perception of the smell/taste and effects are completely subjective there is no way to qualify much less quantify anything using your personal experience... especially since so many variant terpenes smell so similar to the nose but are chemically different none the less. Further complicate things with the veritable cocktail of terpenoids found in cannabis, making... teasing out the individual components of the smell using your nose virtually impossible... and unreliable at best.

let me make an analogy, I can make 20 long island iced teas (an alcohol cocktail with gin, vodka, rum, tequila, an orange liquor and cola) in ten of the cocktails... for the orange liquor I can use triple sec and the other ten I can use grand marnier. Then you being able to ID the triple sec drinks vs the grand mariner drinks by taste with 100% accuracy would be much much easier than accurately ID'ing terpene profiles in cannabis using only your senses.

further more, sensing cannabinoid profiles is impossible, yes you might be able to tell the difference between pure THC, pure CBD, and 50:50 THC:CBD, that is assuming that the cannabinoid ratio is a monogenic co-dominant trait... but seeing as how those are not the only three cannabinoid profiles possible it leads me to believe there are other things going on here besides that form of simple inheritance like either pleitropic genes and or the cannabinoid profile is polygenic (which it most certainly is).

What about all the other cannabinoids... what about a 1:.01 THC:CBD ratio, how would your brain be able to tell the difference between a sample with 21% THC with no CBD and a sample with 20% THC and .2% CBD?

simple answer...
labs are needed to know chemotypes.

progeny testing is needed, to know if the selected parents pass on the polygenic dominant alleles in order to express the desired chemotype in their offspring. (for those who like to read and argue, this does not mean homogeny or lack of variation by the way)

without doing these things, I don't know how someone is actively selecting for chemotype? besides maybe, dumb luck and or using the same true breeding genotypes as everyone else further perpetuating the genetic bottleneck

Anyway, there's quite the discrepancy between what's sold by the big and mighty ones, what's done by the small ones with a big ego on one or a big heart on the other side, and what 'genetics' (or rather crop science) suggests should/could be done.

again, most of the "big guys" in terms of sales numbers... aren't real breeders, so ignorance and mis/disinformation often comes into play. IMO there is only handful, or so, of people that I consider to be real breeders of cannabis; others that I still respect are just more passionate about cannabis than most, have excellent taste and have very very high standards about what makes it into their programs... which I can't say about all or even most "breeder" in todays marketplace.

that doesn't make the small guys making seeds in their closets correct either, people need to not listen to the opinions of so called "experts" and look to the science of both; genetic inheritance which is well established, and the science surrounding cannabis... which is out there just less widely known about and... which is growing all the time.

 

[Only Ornamental]

I agree with you on most points . Suppose even, we are talking about the same but differently...

Though, there's one point where I don't agree. The importance of lab testing... as strange as this may sound from me.
Our problem today is, that we know shit about the things we can test for in cannabis.
A: We don't know what minor cannabinoids do at the feeble concentrations present. An educated guess would be that they do nothing and that weed with 20% THC but either 0, 0.1, or 1% CBD is likely to be identical in its pharmaceutical effects.
B: Regarding smell, no machine can test that. Sure, only machines can help us analyse what's inside an essential oil but they can't tell us the aroma. If we'd knew what the single constituents did, testing would be helpful... With the actual knowledge, it's at best good for consistency testing. I know, there are a lot of effects attributed to mono- and sesquiterpenes. Although, many of the publications are either non-transposable in vitro findings, employ too hight concentrations (>80%), are contradictory, or are more anecdotal than scientific. Essential oil is not very concentrated in cannabis and the single constituents dilute to doses of a few milligram at best. Why advertise 'medicinal cannabis strain due high concentration of limonene' instead of 'smoke whatever you want and drink a glass of orange juice, if all the limonene in your everyday products isn't already enough, to make it medicinal'.

Testing is good, progeny testing mandatory, but it only goes so far in the marketing biz.
Why would people focus so much on 'terpenes' but do way less standard agricultural testing? It's as important to have a plant which grows vigorous and healthy and what do breeders do? How many inoculate their plants with PM or aphids on purpose? Nope, they LOOK at the plant and more subjectively than not decide if the plant's a 'good boy'.
You talk about 'total quantity of secondary metabolite'. Impossible . Who's testing for flavonoids or plant hormones? Why would you want to test for waxes/cuticle?

Oh, and again, testing minor cannabinoids is not chemotype testing. A chemotype test will tell you 'THC chemotype' but not the % of THC and even less something about the minor ones .

Bottom line is, most of today's lab tests are good for potency determination which doesn't necessarily help either; remember the 'entourage effect' we can't explain? At least, machines allow a higher throughput than test smoking. Beyond that, they are funny gimmicks and again marketing. Sorry to disappoint you.

 

[SeedsOfFreedom]

OO, my friend you are dead on! As of this point in time labs have nothing on human tests. Lab tested herb is only good on paper, real world quality is based on smoke. Labs should be a tool for breeders, but when human smoke tests are neglected in favor of lab tests quality will suffer.

 

[oldchuck]

Cannabis is NOT a drug. Cannabis is an herb. I think this is a key fact usually overlooked by everybody. It's like, aspirin is not willow bark. A drug is a specific formulation, either synthetic or natural, with specific targets. A drug is usually only a single active chemical compound not a collection of hundreds of different compounds in quantities that vary even from plant to plant.

This entourage effect is a fascinating idea but, as far as I can tell, only a hypothesis at this point. It makes sense to me but where is some research demonstrating just exactly what the entourage effect is really all about?

So we all use Cannabis in a very imprecise way for whatever purpose. Fortunately it is a very flexible and forgiving plant with almost no hazards so there is little downside to sloppy application except that it won't work for this or that.

I think testing can help. Even if we don't know just how the various components interact we can benefit simply by correlating what works for this or that with test results. I'm not talking about how sweet a bud smells or how high it gets you but what works to quiet seizures or eliminate back pain.

 

[Sam_Skunkman]

I agree with you on most points . Suppose even, we are talking about the same but differently...

Though, there's one point where I don't agree. The importance of lab testing... as strange as this may sound from me.
Our problem today is, that we know shit about the things we can test for in cannabis.

Or at the least most do not know.

A: We don't know what minor cannabinoids do at the feeble concentrations present. An educated guess would be that they do nothing and that weed with 20% THC but either 0, 0.1, or 1% CBD is likely to be identical in its pharmaceutical effects.

I have tried many of them, some with THC to see if it moderated the THC effects. To get high you want high THC and the right terpenes for the effects and taste you prefer. No other Cannabinoid makes THC better, unless you call what CBD does to THC better because it lasts longer, also with delayed onset, and reduced peak experience.

B: Regarding smell, no machine can test that. Sure, only machines can help us analyse what's inside an essential oil but they can't tell us the aroma. If we'd knew what the single constituents did, testing would be helpful... With the actual knowledge, it's at best good for consistency testing. I know, there are a lot of effects attributed to mono- and sesquiterpenes. Although, many of the publications are either non-transposable in vitro findings, employ too hight concentrations (>80%), are contradictory, or are more anecdotal than scientific. Essential oil is not very concentrated in cannabis and the single constituents dilute to doses of a few milligram at best. Why advertise 'medicinal cannabis strain due high concentration of limonene' instead of 'smoke whatever you want and drink a glass of orange juice, if all the limonene in your everyday products isn't already enough, to make it medicinal'.

You are so wrong about all this. If you had ever smoked 100% pure THC and then the same amount of pure THC spiked with a single terpene of the right kind, you would not say it.
You need to inhale the limonene with the THC to modify the THC effects. Or are you a believer of the eat a mango when you smoke, to get myrcene, and higher from the smoke?

Testing is good, progeny testing mandatory, but it only goes so far in the marketing biz.
Why would people focus so much on 'terpenes' but do way less standard agricultural testing? It's as important to have a plant which grows vigorous and healthy and what do breeders do? How many inoculate their plants with PM or aphids on purpose? Nope, they LOOK at the plant and more subjectively than not decide if the plant's a 'good boy'.
You talk about 'total quantity of secondary metabolite'. Impossible . Who's testing for flavonoids or plant hormones? Why would you want to test for waxes/cuticle?

I think you are misjudging the importance of terpenes in breeding by most people that make and sell seeds, few breed based on terpenes, that I know of. They will. As for the flavonoids if you eat it they may well have effects, but for smokers I doubt it.

Oh, and again, testing minor cannabinoids is not chemotype testing. A chemotype test will tell you 'THC chemotype' but not the % of THC and even less something about the minor ones .

Bottom line is, most of today's lab tests are good for potency determination which doesn't necessarily help either; remember the 'entourage effect' we can't explain? At least, machines allow a higher throughput than test smoking. Beyond that, they are funny gimmicks and again marketing. Sorry to disappoint you.

I disagree, Cannabinoid profiles and %'s along with terpene profiles and %'s are the future and are just beginning to be used. I look forward to being so familiar with the 130+ terpenes that all I have to do is read the Cannabinoid and terpene label and I can predict the potency, taste and smell of any bud or resin. I am beginning do it now.
And I do agree that labs are required to help winnow down the prospective keepers from a crop of 10,000 from seeds, you can not smoke them all. It is not enough to just lab test the potency of the THC, it is the right terpene profiles and high terpene %'s with high THC that you want, with all the traits required for a good agricultural crop in the area you want, or in a building if that is what you really want...
-SamS

 

[VerdantGreen]

Sam, do terpenes burn/vaporize at the same temps as THC?

i was wondering why the high from vaporising is so different from burning - makes me wonder if you get more of a pure THC high from vaping without the modifyning effect of some of the terpenes...

VG

 

[Sam_Skunkman]

One of the biggest differences with smoking vs vaping is the amount that you can smoke in one breath is way bigger then the same amount vaporized into 1 or 2 bags that have multiple breaths in each bag.
Big difference.
I really only use a vape for research reasons. They just don't get me off the same.
But I am happy some people like and use them.
-SamS

 

[Only Ornamental]

Strictly spoken, medicinal plants, the instant they are turned into a 'consumable' form (dried, extracted etc.), are regarded as 'drug', especially in pharmacy (an old habit) .
BTW aspirin is a bad (or good?) example, because the active ingredient acetyl salicylic acid has many targets and hence a plethora of pharmacological activities beyond 'killing pain' (some of which are still poorly understood).

The 'entourage effect' in phytopharmacy and pharmacognosy is generally termed 'matrix effect' or regarded as 'synergistic or super-additive effects' if several known active constituents are contained, respectively. It is a well known, rather infamous, observation commonly seen with plants (mostly with plant extracts tested in in vitro assays). Cases where the underlying interactions could be elucidated are very scarce (e.g. Ayahuasca, which is actually a mixture of two plants), often caused by non-specific interactions with the used test system, whereas those where reconstitution experiments fail (hence, where we can't explain it) are the norm. This whole thing gets even more complicated for plants where useful in vitro screenings or even animal assays are lacking, like in the case of cannabis.

For me (based on knowledge and experience in this field), the 'entourage effect', and Sam will disapprove, is a hypothesis and even more so a hype until proven otherwise.

At the moment, most of the currently employed tests should be used to determine markers, to track consistency and therefore quality (given that the parental line or variety of comparison already express the desired quality). We can not use it to transpose from one plant good against illness XY to another variety concluding that the latter one will or will not help against the same illness simply because there is no connection between obtained data and observed effects. Well, there might indeed be something; though only testing now will hopefully help somewhen in the future.

A point I don't like is the focus on 'hypes' instead of 'usefulness'.
A variety is praised to have buds so heavy they bend the branches and need support: Maybe the breeder just selected towards a variety with a low fibre content or bad fibre quality and not big buds? Testing his plants also for fibres the way it's done in hemp (i.e. Bredemann principle) would have shown him which one it is. But you can't advertise a variety as 'buds bend over due low fibre content' (even though this might imply that the plant has more resources available for flower and resin production LoL).

Although cannabis is mostly smoked/vaped/inhaled, the rather high flavonoid content gets completely neglected beyond affecting colouration. People focus on volatile 'terpenes' though some are more harmful than useful (e.g. allergies, topical irritation by pinenes) and most are even present in near homoeopathic doses whereas flavonoids are present at pharmacologically relevant concentrations and have proven effects (and an even bigger bunch of effects falling into the category of essential oils but often with some more reliability) when eaten or applied topically for example as a cream or ointment.
Apropos healthy terpenes; I always wondered why nobody talks about beta-caryophyllene (BCP). This is likely the only one which shows true activities and is, at least in some hemp varieties, concentrated enough. Its activities are under others mediated via the CB2 receptor, it acts additive to THC regarding modulations of the immune system and inflammation. My own personal experience (consumption, not lab stuff ) points even towards a stronger effect of BCP than THC against cough, sore throat, and feverish conditions. Common hemp seems to help me more against inflammatory-related little ailments than any drug type cannabis I tried so far. Could be CBD, but there's no data available on immunomodulation or effects on inflammatory diseases (apart from IBD).

And now the labs start offering 'gene tests'...

 

[Only Ornamental]

I disagree, Cannabinoid profiles and %'s along with terpene profiles and %'s are the future and are just beginning to be used...
-SamS

Precisely, the FUTURE, not the present! THAT'S what I'm talking about. There is certainly something, but we don't know what that is and until then...

Regarding the 'entourage effect': Sam, no need to repeat yourself , I know what you mean and I can see your point. I don't believe neither in it nor 'against' it. It's just that the whole thing doesn't add up. It shouldn't matter if you smoke additional terpenes or eat/drink them, there should be a bigger difference between smoked and eaten cannabis... science tells me that the effect might have something to do with smell and olfactory perception rather than something from academic medicine. But then, all the nice profiles won't help more than your nose .

Besides, you're right, flavonoids just burn to cinder when smoked... at best give the smoke a hint of berry flavour.

 

[Only Ornamental]

Sam, do terpenes burn/vaporize at the same temps as THC?

i was wondering why the high from vaporising is so different from burning - makes me wonder if you get more of a pure THC high from vaping without the modifyning effect of some of the terpenes...

VG

Don't know where exactly I've read about that; there's a publication (you may use Pubmed.com to find it yourself) wherein they analysed the constituents of eaten, smoked, and vaporised herb and, if I'm not mistaken, did some resorption studies too. Astonishingly, they found that smoke was 'purer' (less stuff inside) than vapour.
The different constituents of essential oils have also very different boiling points and even more important different gas pressures. When smoking a joint, you create a temperature gradient between room temperature and incandescence plus create stream (water vapour) from residual water and as a product of the burning process. Both help to optimally evaporate and co-evaporate, respectively, the whole spectrum of mono- and sesquiterpenes. On the other hand, vaporisation may be too hot for one but not hot enough for another.

 

[Infinitesimal]

OO,
I was thinking in terms of genetics and selection when discussing terpene and cannabinoid profiles... not their medicinal efficacy, which would be more a part of a breeding projects goal. Identifying which chemicals or cocktails their of produce the best results and the genes responsible for their synthesis seems like very important data to have whether the goals are medicinal recreational or just for fragrance (I have a plant that I will grow just so I can sniff it )

I am not down playing our experience of taste and smell as that is a great part of enjoying cannabis in my opinion. Just that the only way I can see for someone to affirmatively say anything about terpene and cannabinoid profiles and levels, they need to be analyzed and correlated to the smoking experience. Then through looking at data regarding the best smoking plants and the correlating terpene/cannabinoid profiles... we should be able to make certain distinctions regarding plant vs plant of the same variety.

Sam,

can premature males be tested, to see if the profiles match the best females from the population?

if there is enough resins, is would seem very helpful to know.

 

[Sam_Skunkman]

OO,
I was thinking in terms of genetics and selection when discussing terpene and cannabinoid profiles... not their medicinal efficacy, which would be more a part of a breeding projects goal. Identifying which chemicals or cocktails their of produce the best results and the genes responsible for their synthesis seems like very important data to have whether the goals are medicinal recreational or just for fragrance (I have a plant that I will grow just so I can sniff it )

I am not down playing our experience of taste and smell as that is a great part of enjoying cannabis in my opinion. Just that the only way I can see for someone to affirmatively say anything about terpene and cannabinoid profiles and levels, they need to be analyzed and correlated to the smoking experience. Then through looking at data regarding the best smoking plants and the correlating terpene/cannabinoid profiles... we should be able to make certain distinctions regarding plant vs plant of the same variety.

Sam,

can premature males be tested, to see if the profiles match the best females from the population?

if there is enough resins, is would seem very helpful to know.

I would transform the male to a female and then smoke or lab test it. I have done this it is easy.
It is not so good to see the female bud form or yield but works great for terpene and cannabinoid profiles, really amazing.
https://www.icmag.com/ic/showthread.php?t=99597&highlight=males+transformed+female

 

[Only Ornamental]

OO,
I was thinking in terms of genetics and selection when discussing terpene and cannabinoid profiles... not their medicinal efficacy, which would be more a part of a breeding projects goal. Identifying which chemicals or cocktails their of produce the best results and the genes responsible for their synthesis seems like very important data to have whether the goals are medicinal recreational or just for fragrance (I have a plant that I will grow just so I can sniff it )

I am not down playing our experience of taste and smell as that is a great part of enjoying cannabis in my opinion. Just that the only way I can see for someone to affirmatively say anything about terpene and cannabinoid profiles and levels, they need to be analyzed and correlated to the smoking experience. Then through looking at data regarding the best smoking plants and the correlating terpene/cannabinoid profiles... we should be able to make certain distinctions regarding plant vs plant of the same variety.

Sam,

can premature males be tested, to see if the profiles match the best females from the population?

if there is enough resins, is would seem very helpful to know.

Agreed. Though, I suppose that correlating a subjectively perceived and elusive high-feeling which also depends strongly on set and setting among other things to a chromatogram. I'm not saying it were not possible but our background knowledge is simply not present at a favourable amount, so to speak.
BTW I tried this sort of things myself but with different plants and a bunch of models (e.g. whole blood, cell lines, enzymatic assays); even though my preconditions were better, it still got very complex and complicated very fast. Then it came down to statistics and and numbers... A PCA could have been tried but therein one often does not know which constituent's where. In my case this would have been bad, in case of cannabis it might be favourable. But what exactly do people do with their chromatograms and their %? This are only raw data, numbers, nothing more; they have to be treated some way to be useful. Could anybody tell me how? It will only be easy like 'high X, low Y' in a very few cases.

There's not much to gain with such complex challenges and therefore many abandon them from the start. This in turn keeps the amount of knowledge low and obviously discourages others to work in the corresponding field... a vicious circle.
I wish everyone luck (and success) who tries!

Forgot to mention:
Looks like the essential oil and to a lesser extend cannabinoid composition of sessile glands during vegetative growth is different than the one from stalked trichomes during flowering.
Furthermore, many hemp/cannabis varieties during vegetative growth show about 0.6% THC+CBD (seems as if a good part came from the tissue and not glands). Testing in vegetative growth (male or female) can be helpful for forensics (chemotyping 'hemp v.s. cannabis') but doesn't correlate enough with final concentrations (potency testing 'legal v.s. illegal').

 

[Sam_Skunkman]

Hey all. New to icmag, although I have used the forums as a source of info for a while. I decided to join after seeing some familiar and knowledgeable people on here from other boards. I posted this info over on GC and got very little interest. I see the breeding sub forum is very big over here and I figured I would post it over here and see if it received any better.

Its one hell of a long post as it was multiple posts on another board. Things may not quite seem in order, or it may seem like it bounces around a bit. Sorry about that but I'm not retyping all of that so you have to just bear with me.

Beware! Your eyes are about to be violated by a wall of words, hang in there though, I feel most of the info is easy to digest.








So first and foremost a disclaimer: I'm not a genetics major, or professor, nor am I actively involved in the breeding of any plant or animal at the moment. Just a guy that has studied up on the subject enough to possibly shed some light on a confusing topic. You are welcome to disregard any information henceforth and assume I am full of shit. If you have a piece of valuable, pertinent information feel free to post it. If you are a genetics student or professor and feel the verbage or information presented here is not good enough, blow me. I am speaking in generalities to make the information listed comprehendable by novice growers and breeders, not to provide geneticists an encyclopedic reference on the subject. Textbooks have been written thoroughly covering the subject already.

Now we can get started,

Again this is a generalized explanation to keep things (kinda) simple.
Genetics is, in its basic form, a study of genes and how they interact. Genes are the basic units of heredity, coming in bundles called chromosomes. Genes come in pairs and are arranged in a linear fashon along chromosomes like beads on a string. It is now known that chromosomes are just big dna molecules, containing millions of gene pairs. The location (locus or plural loci) of these paired genes (called allele or plural alleles) along a given chromosome and how chromosomes (and in turn how alleles) are paired, gives rise to all the variation in a given species. Cannabis has 10 pairs of chromosomes, making a total of 1024 possible chromosome combinations (calculated 2^n whereas n= the number of chromosome pairs) compared to humans who have 23 pairs of chromosomes making 8,388,608 possible combinations and domestic dogs who have 39 chromosome pairs bringing rise to 549,755,813,888 possible chromosome combinations! Chromosomal inheritance is universal in life forms and even though there is a proportional decrease in possible combinations compared with the number of chromosome pairs, there is still an abundance of variation in cannabis.

There are some chromosomes that are involved in reproduction, we know them as the X and Y chromosomes, these chromosomes carry sex-linked traits, an example would be color blindness in humans. Cannabis has 9 pairs of "autosomal" or, non sex chromosomes and 1 pair of 2 sex linked chromosomes, either an X combined with an X, making a female or an X combined with a Y for males.

Meiosis is reproductive cell division where a complete (diploid) set of chromosomes is divid ed into half (haploid). The joining of two haploids again creates a complete set of chromosomes and a new organism is born. Each germ (sex) cell starts out with a diploid set of chromosomes, one of each set coming from each parent. There is never any discrimination as to how the chromosomes are divided, as long at its half, and there is no discrimination amongst the haploids and how they reform to diploid, the only priority being that the diploid is divided in half and the haploid receives a complimentary set of chromosomes to once again become diploid. Meiosis randomly separates the parental pairs and fertilization restores them randomly to their diploid state. Their is also the ability for chromosomes during meiosis to "swap"or "mix and match" some information. This reciprocal exchange of segments of genetic material between two chromosomes places genes in the same sequence and location on the chromosome, but in new combinations. Things can get a little confusing here and I don't want to write a novel so suffice it to say the way chromosomes are divided during meiosis creates the random character of inheritance, this allows us a statistical predictably of traits, giving us a bit of control over said traits.

There are four modes of inheritance, autosomal (non sex-linked) dominant, autosomal recessive, sex-linked recessive, and polygenic (meaning more than one gene is responsible for it's inheritance or expressivity). The modes of inheritance that I will focus on are autosomal recessive or dominant. These are simple to understand and will give you a foundation on the basics. I gave a basic definition of allele earlier, let me elaborate.

The term allele is used to define two genes situated at the same position (locus) on homologous (matched or paired) chromosomes. Alleles are both sides of the same coin, alternate forms of the same gene. The same allele that control how tall somethig may be, paradoxically controls how short it will be. It is again the possible paired combinations of the two forms of a given gene that control what trait will be expressed. There are two forms of alleles at a given locus, one is dominant (denoted with an upper case letter like A) and one is recessive (signified by a lower case letter, a). Thus you have three combinations for the alleles, AA, Aa, aa. In this example I will use height as the trait for simplicity, if the dominant form for the allele controlling height is short stature, written "A", then the recessive form of that allele producing more height is written "a". AA is an example of double dominance and because they are a matched pair they are called homozygous, this double dominance means that the organism will be short, and breed true for the short trait, never producing direct offspring (daughters and sons) that are tall. Aa is a combination that means the organism will be short, but be a carrier for the genes that would produce a taller stature, being an unmatched pair they are called heterozygous. The combination aa would also be considered homozygous because they are a matched pair, but are double recessive, this doubling up of the recessive allele will produce an organism with a higher stature than the majority of the population. The only way a recessive allele can be expressed is if it is matched (homozygous) with another recessive counterpart. An easy way to illustrate the probability of inheritance for a certain trait is a diagram called a punnett square, a simple tool to help visualize the probability of progeny that will express a certain trait. A quick Google search will show how to properly use a punnett square for anyone interested.

So now we see that there is a level of predictably for the inheritance of traits. If a double dominant parent is taken to a double recessive parent,(AA x aa) none of the offspring will express the recessive trait, they all however will carry the recessive trait and have the ability to produce progeny expressing the recessive trait (100% of the offspring will be Aa from a [AA x aa] cross). If a double dominant parent breeds with a heterozygous parent that has both the dominant and recessive version of a given allele, (AA x Aa) then all the offspring will express the dominant trait and only 50% of the progeny will be carriers for the recessive trait, the other 50% will be homozygous and true breeding for the dominant trait (50% AA, 50% Aa). If two heterozygous parents (Aa x Aa) are bred, you will finally find offspring expressing the recessive trait, (25% will be double dominant AA and true breeding for the dominant trait, 50% will express the dominant trait but be heterozygous and carry the recessive trait Aa, the final 25% will be double recessive aa and express the recessive trait without being a carrier for the dominant trait. Remember if a dominant allele is present the trait that allele is "coded" for will be expressed, you cannot express a recessive trait and also carry the dominant, if the dominant allele is present it will be expressed and mask the recessive trait.

This brings us to the most abused genetics jargon in the cannabis community, genotype and phenotype. Phenotype is what is physically observable in a specimen, and in genetics, includes nurture and nature. That is to say if a specimen does not reach its genetically predisposed height due to malnutrition, its height or lack thereof is still part of its phenotype. Genotype is all the genetic information contained in a specimen, dominant or recessive, observable or not. A given specimen in their genotype may contain the information to produce multiple, distinct, phenotypes, but because of the relationship between its inherited alleles, and the fact it can only display one physical manifestation of the genome, can only express one pheno.

Now that we have a better understanding of some of the modes of inheritance, and how genes interact with eachother to produce a certain trait, we can now examine the methods that breeders use to produce strains with set, defined, traits, and are true-breeding for those selected traits. There are only a few terms that have been coined by the breeding community to reflect some sructure or template for their breeding. There is simply inbreeding and out-crossing, that's it. You may have heard of backcrossing, line breeding, in line breeding, inbreeding, cubing (a big one used often by cannabis breeders) or any other format on which to structure your breedings. All of the previously listed terms are a way of saying inbreeding, and if its not inbreeding its an outcross, no exceptions. All breeds of dogs and furthermore all "strains", "bloodlines", "sub species", however you would like to refer to them, are inbred and their uniformity and true breeding nature are a direct result of inbreeding.

Now I know your thinking, "inbreeding is bad right?" "I thought inbreeding made diseases and deformities." Sorry but your wrong, inbreeding has a stigma in our society due to religious and moral views. I'm not suggesting you should start bumpin uglies at the family reunion, but it happens in nature all the time, humans are even inbred. Don't believe me? Do some quick math, take your family tree and trace it back far enough, you will find that at some point there are more ancestral places in your family tree then there were people on the planet at that time.

Since we have discussed how traits are inherited the idea of using closely related specimens for breeding kinda makes sense. When working with specimens that share a common ancestry, you are more likely to double up on certain alleles. The closer related the greater the chance that some of the progeny will inherit matching alleles from their parents that they themselves inherited from a common ancestor. Working within a family you can be more sure that traits will be inherited from one generation to the next, and choosing a closely related mate for a planned breeding assures you that you have a greater chance at setting a selected trait in your line by creating homozygousness at the chromosome. Inbreeding also allows you to perform test breedings, helping you better understand the genotype of the strain you are working with and more importantly, the genotype of your breeding stock, selecting mates not just on their observable traits but their potential genetic contribution to the cross. This is where the use of a punnett square and some deductive reasoning will really aid you in learning about your brood stock. Like we said earlier, inheritance is predictable, and knowing what genes interact with eachother and the probability of a trait being expressed, you can deduce much about the population you are working with.

One thing to always remember is that inbreeding neither adds nor subtracts from the line. It simply doubles up on what is genetically there, creating new possibilities. Inbreeding is not bad, nature is imperfect! Inbreeding does not create problems, deformities, or disease, but it does rapidly bring masked recessive traits to the surface where they can be selected for or against, recessive doesn't always mean bad, it means its recessive. Inbreeding can make an abundance of problems or it can rapidly set desirable traits on the line, making homozygousy, and a true breeding offspring. If an insestual breeding occurs between two specimens and a masked genetic deformity or trait rears its ugly head, do not fear! As we learned earlier the same breeding that will produce offspring affected by a recessive genetic trait will also produce a predictable ammount of offspring completely unaffected by the recessive trait and they will not be carriers for the trait either. A double edged sword that must be respected and used wisely.

Inbreeding depression is a term used when inbreeding is abused and a general lack of vigor, fecundity, and health is lost throug h successive generations. When this occurs breeders usually look for an outcross to bring the inbreeding coefficient down and promote vigor and fertility. Inbreeding depression can happen to any organism but inbreeding is not to blame. Again nature is imperfect, you doubled up on a piece of genetic information already in your line, and now you have a problem, inbreeding didn't cause the problem, it just made it visible. Now that a negative trait has been expressed, its not necessarily time to find an outcross, just select against that trait for future breedings. There are strains of lab mice that are a result of 100s of generations of brother - sister breedings to keep the line uniform and genetically, nearly identical for testing purposes of pharmaceuticals. These lab bloodlines have exhibited no apparent loss of health, vigor, or fertility, with an inbreeding coefficient (a measure of to what extent a specimen is inbreed written in percent) of 95% and in some cases higher. How is this? The original breeding stock was of superior quality, and the breeders culling process was thorough and rigorous, only selecting the best specimens for future breedings.

I wanted to take a quick minute to write something up about sex linked traits before going on to hermaphrodism, so here goes.

Sex linked traits are referring to alleles located on the sex chromosomes, the X and the Y. The chromosomes that determine gender are unique and easily distinguishable from each other, two Xs make a female and an X and a Y make a male. There are X and Y linked traits, some may be good, others bad, and others absolutely necessary (in mammalian females the ability to lactate comes from the pairing of alleles on the X chromosomes). Many of the negative sex linked traits are recessive, and therefore associated with males, ill explain this later. The X chromosome is larger than the Y and contains more information than the Y, much of this extra information is related to reproduction.

Imagine alleles as blueprints for a construction site. When referring to negative recessive traits, we can pretend the recessive allele is a bad copy of blueprints. We will say each crew gets a pair of blueprints (pair of alleles), if a crew gets a quality and complete set of blueprints (AA), the job will be done properly. Even if they get one bad copy of the blueprints (Aa), they can still get the job done fine, but if they get two bad copies of the blueprints (aa), the job will not get done, or it will not be done correctly. Of course this example only works when referring to negative recessive alleles, but its a fairly good illustration. It is the same idea with negative sex linked traits, and this is why most negative sex linked traits affect males and not females.

Let's examine color blindness in humans, women and men can both be colorblind, but most people that are affected are males. This would make you think it is a Y liked trait, not an X linked, but its an X linked trait and its going to make more sense in a minute. Like the construction example, if there are a bad set of blueprints the job won't be done, or it will be done incorrectly. Males have one X and one Y, females have no Y chromosome but can still be color blind, so it can't be Y linked. If a male inherits his affected X chromosome from one of his parents, he has no other X chromosome to mask the color blindness, and will be affected. If a female inherits an affected X chromosome from her parents, chances are she will inherit a good copy of an X chromosome from the other parent, and although she will be a carrier, like autosomal traits she will not be affected. A male cannot be a carrier for an X or Y linked trait and not be affected, he only has one copy of each. A female can't be affected by a Y linked trait she has no Y chromosome, and for her to be affected by a sex linked trait she would have to be homozygous for the affected allele on the X chromosome, and she had to have inherited a defective X chromosome from BOTH parents meaning her father was affected as well. In planned breedings you would not breed a specimen affected by a negative trait, so affected females are rare. For a male to be affected for a Y linked trait, he must have inherited that Y from his father, his mother has no Y to contribute. If he is affected by a Y linked trait then so was his father whom he inherited it from, and again in a planned breeding you would not breed an affected specimen. This is why the most common negative sex linked traits are X linked, they are inherited from the maternal side not the paternal, but only males are affected when two unaffected specimens were bred. The female was the carrier but only some of her sons will be affected, some of her daughters however like her will be carriers. Because sex linked traits are simple recessive a punnett square can also be used in these scenarios to determine the probability if inheritance for a trait.

Cannabis is an annual, dioecious, angiosperm. Well what the fuck does that mean? It's a fancy way of saying pot lives its whole life cycle in one year, it has distinct male and female plants, and pot is like most plants in the plant kingdom, reproducing by sex and producing seed and flowers or fruit (bud). About 80% of all angiosperms are hermaphrodites, known in horticulture as having "perfect flowers", meaning each individual flower has staminate (male), and pistilate (female) parts. About 12% of angiosperms are monoecious, meaning that the same plant produces both male and female flowers, either at the same time or one then the other, but the flowers are distinct from each other, either being just male or just female. The remaining 8% are dioecious, meaning there are two distinct sexes in the species, and plants are either male or female. Cannabis is considered subdioecious, meaning individual specimens may produce flowers that are not clearly male or female, when the majority of the species population is dioecious and either distinctly male or female.

So when you think about it, the properties and tendencies of our favorite plant is actually fairly rare in the plant kingdom, being a member of a class of plants that only makes up a few percent of angiosperms. It is accepted that all angiosperms today developed from a common ancestor that had a favorable genetic mutation, and unlike any other plant on the earth at the time reproduced not by spores or cloning but by sex, and this first example was hermaphroditic. This explains why the overwhelming majority of angiosperms are hermaphrodites, and why cannabis exibits these tendencies.

Now, in regards to breeding and hermaphrodites, I only have a few things to say. I must admit that out in he wild, there is probably a few populations of cannabis that are all naturally hermaphrodites, and even though mother nature is cruel and the population is a result of a herm breeding or even selfing, the population thrives.


Can you list one naturally all hermaphrodite population out in the wild? And not from the hand of man like in Thailand where the cultivation of sinsemilla has allowed any seeds made and found in the sinse are from intersex females with a few male flowers to be produced in the crop. Use the seeds and you will get intersex progeny, the more used and the longer the higher the % of intersex. Real sinse farmers in Thailand do not use seeds found in sinse crops they get seeds from professional seed makers that avoid intersex seeds and any intersex plants when they make seed crops.


Herm breeding in nature will not lead to the demise of the population or species, like we said earlier 80% or all angiosperms are hermaphrodites, some are self sterile but still others are not. Hermaphrodism is not an epidemic to cannabis, its common in nature. What we in the pot community seem to always forget it that cannabis does not grow so we can get high. The beauty of plants is the art of biochemistry, and the natural creation of unique complex molecules. Cannabis happens to make THC, and that's why we grow it. We seem to think if something does not increase the drug quality of cannabis, it must not be good for it. We forget just as much cannabis has been grown in this world for it's textile uses, or as a food, as it has been grown for medicines and intoxication.

Are you saying that hemp varieties are hermaphrodite? I don't think so, many are monoecious, all made by man and maintained by man.

My point in all this is that cannabis will always exhibit this herm trait to some degree in at least some of the species. It's not the end of the world or our favorite plant, but with the intent of increasing the drug quality of cannabis, herm breeding should be obviously avoided. A self breeding genetically is the closest inbreeding that can be performed, but it still follows the rules of heredity and genetics. The problem with selfing is it brings forth recessive traits and rapidly and abruptly sets them in the progeny, making it difficult to slowly select for good traits and cull the bad ones. We want to grow knock your socks off sensimillia, and for those purposes it would not be wise to incorporate hermaphrodites into a breeding program.

I do not think all Cannabis is intersex, I am pretty sure in fact as I have female clones that will not express intersex regardless of any/all environmental stresses, I have tried and tried, most will if treated with STS but that is quite different as it will not happen in nature. I even have a few that will not make male flowers even if treated with STS, or at the most they make male flowers that are functionally sterile, the pollen is sticky and does not dehisce and drop, it can be used with a q-tip but is a pain to use.
-SamS

 

[Sam_Skunkman]

Agreed. Though, I suppose that correlating a subjectively perceived and elusive high-feeling which also depends strongly on set and setting among other things to a chromatogram. I'm not saying it were not possible but our background knowledge is simply not present at a favourable amount, so to speak.
BTW I tried this sort of things myself but with different plants and a bunch of models (e.g. whole blood, cell lines, enzymatic assays); even though my preconditions were better, it still got very complex and complicated very fast. Then it came down to statistics and and numbers... A PCA could have been tried but therein one often does not know which constituent's where. In my case this would have been bad, in case of cannabis it might be favourable. But what exactly do people do with their chromatograms and their %? This are only raw data, numbers, nothing more; they have to be treated some way to be useful. Could anybody tell me how? It will only be easy like 'high X, low Y' in a very few cases.

There's not much to gain with such complex challenges and therefore many abandon them from the start. This in turn keeps the amount of knowledge low and obviously discourages others to work in the corresponding field... a vicious circle.
I wish everyone luck (and success) who tries!

Forgot to mention:
Looks like the essential oil and to a lesser extend cannabinoid composition of sessile glands during vegetative growth is different than the one from stalked trichomes during flowering.
Furthermore, many hemp/cannabis varieties during vegetative growth show about 0.6% THC+CBD (seems as if a good part came from the tissue and not glands). Testing in vegetative growth (male or female) can be helpful for forensics (chemotyping 'hemp v.s. cannabis') but doesn't correlate enough with final concentrations (potency testing 'legal v.s. illegal').

When we tested veg females and flowered females of the same clone they had the same ratios of Cannabinoids in their profiles, except for CBC. What reference did you get this info from? Or is it work you did your self?
-SamS

 

[ozza]

And what's your take on it?

exactly as the description actually, good uniform plant. Very sweet Fruity.

 

[Only Ornamental]

When we tested veg females and flowered females of the same clone they had the same ratios of Cannabinoids in their profiles, except for CBC. What reference did you get this info from? Or is it work you did your self?
-SamS

It's from a publication. If I can find it again, I'll tell you.
You're right, the ratio between THC, CBD, and if at detectable amounts present also the V's are the same no matter what.

 

[Only Ornamental]

Couldn't find the one about essential oil (yet) but found one on cannabinoids:
Nizar Happyana et al. Analysis of cannabinoids in laser-microdissected trichomes of medicinal Cannabis sativa using LCMS and cryogenic NMR, Phytochemistry, 2013, 87, pp. 51–59

 

[Only Ornamental]

Here's one that might help... though you know it already:
C. Meier and V. Mediavilla, Factors influencing the yield and the quality of hemp (Cannabis sativa L.) essential oil, Journal of the International Hemp Association, 1998, 5(1), pp. 16-20