To which I responded:
- a plants dna can be altered by a virus. HIV - a human virus which is sexully transmitted can be passed on to offspring because it becomes part of the dna. when scientists genetically engineer crops, they use a disabled virus as the carrier. once the new crop with the new trait(s) is released, they can pass the new genetic trait on to offspring.
'Genetic drift' is often used in biology to describe what happens as allele frequencies change randomly from generation to generation.
When cloning there is a different kind of 'genetic drift'. This is a drift caused by the lack of random changes from generation to generation, as the plant is reproducing via mitosis with adventitious roots.
That is the start of the degradation Outlook....You will be fine for a while, but potency, vigor, and yeild will drop off over time. The reason being is that indoors we simulate nature and manipulate it. MJ is an anual plant that has a certain lifespan built into it based on photoperiod sigantures. Once a plant has gone into it's flowering mode this signals that it is to reproduce then die. I'm not saying it can't be done as I have both cloned flowering plants and revegged flowered plants for a 2nd harvest....I'm saying that it will trigger changes in the plant that are not desirable and the plants will eventually degrade.
Have plant Y chromosomes degenerated?
Before using plants to study genetic degeneration, we need to know if their Y chromosomes are indeed degenerating. The evidence from the best studied species suggests some degeneration. Rumex acetosa Y chromosomes are heterochromatic (Clark et al, 1993; Réjon et al, 1994; Lengerova and Vyskot, 2001). On the other hand, DNAse digestion experiments suggest transcriptional activity of this Y chromosome (Clark et al, 1993), though this could be due to the presence of dispersed repetitive sequences that are transcribed, such as transposable elements. The high frequency of chromosome rearrangements in this species (Wilby and Parker, 1988), and variability of its Y chromosome morphology (Wilby and Parker, 1986), are consistent with such a possibility, but it has not yet been tested. Some X-linked mutations are not masked by the Rumex Y chromosome (Smith, 1963), ie males are hemizygous for this region, like classical sex-linked loci in many animals.
In Silence latifolia, the two X chromosomes differ in the time of replication, as might be expected if one of them is transcriptionally silenced, and they appear to be differentially methylated, possibly indicating that dosage compensation is occurring by X inactivation in females (Vyskot et al, 1999). Gene expression from Y chromosomes is suggested by estimates of methylation levels (Vyskot et al, 1993), which may imply that many Y-linked genes have not degenerated greatly, if at all (though again the possibility of transposons cannot be excluded). The large size of the Y chromosomes in S. latifolia and dioica (Costich et al, 1991) and many other dioecious plants (Parker, 1990), also suggests that plant Y chromosomes have accumulated repetitive sequences, which have been found on Y chromosomes of S. latifolia (Donnison et al, 1996; Zhang et al, 1998; Lardon et al, 1999) and R. acetosa (Réjon et al, 1994). So far, however, abundances are mostly similar on the X and autosomes (Clark et al, 1993; Donnison et al, 1996; Scutt and Gilmartin, 1997). Thus the evidence is inconclusive, and the nature and range of kinds of such sequences is currently almost totally unknown.
In most studied species with heteromorphic sex chromosomes YY genotypes are inviable (see above), as are androgenic haploid plants of S. latifolia, with only a Y chromosome (Ye et al, 1990), while X-haploid plants are viable. However, the viability and fertility of occasional YY dihaploids (Vagera et al, 1994) argues against complete loss or inactivation of genes, presumably because increased gene dosage permits survival. Finally, female biased sex ratios in both S. latifolia (see Correns, 1928, but also Carroll, 1990) and Rumex acetosa (Smith, 1963; Wilby and Parker, 1988) as well as other dioecious species suggest that pollen grains with Y chromosomes grow more slowly than X-bearing pollen. This suggests that plant Y chromosomes have reduced gene functions (Smith, 1963; Lloyd, 1974), though segregation distortion has not been ruled out (Taylor, 1994).
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Molecular genetics of plant Y chromosomes
Our understanding of the evolution of plant sex chromosomes and sex determination should be advanced by the use of molecular markers, so several groups are searching for these. The region containing the sex determining loci must initially have been fully homologous between the two alternative chromosomes. One goal of studies of plant sex chromosomes is therefore to test for homology. Both X- and Y-linked markers are now being discovered in plants with and without heteromorphic sex chromosomes (eg Testolin et al, 1995; Harvey et al, 1997; Polley et al, 1997; Zhang et al, 1998; Mandolino et al, 1999). Most markers are, however, anonymous, and cannot tell us which X-linked loci have homologues on the Y chromosomes and which do not.
Isolation of male-specific cDNAs from developing flower buds or reproductive organs has not yet led to discovery of sex determining genes (Matsunaga et al, 1996; Barbacar et al, 1997), probably because sex-determination happens very early in flower development (Grant et al, 1994), so the genes identified are controlled in response to sex, rather than the controlling loci. Genes known to be important in floral development, including the homoeotic MADS-box genes also appear not to have direct roles in sex determination (Hardenack et al, 1994; Ainsworth et al, 1995). This is not surprising, as these mutations change floral organ identities, whereas in unisexual flowers apparently normal reproductive organs merely stop developing, as predicted by the genetic model above.
Both X- and Y-linked expressed loci have now been identified in S. latifolia. One approach is to directly search for sex-linked genes (Guttman and Charlesworth, 1998). This has identified the X-linked MROS-X (male reproductive organ specific) gene and its Y-linked homologue, MROS3-Y, which appears to have degenerated. MROS3-Y contains only a short region of homology to the MROS3-X sequence. This region has been evolving in a neutral manner, with a ratio of silent to replacement substitutions, Ka/Ks, of 0.974, close to unity, as expected for a sequence evolving without selective constraints (Nei, 1987).
Another approach has isolated Y-linked genes present in mRNA populations from S. latifolia male flower buds. Two gene pairs have so far been characterised. Based on sequence similarity to other genes, the SlX/Y1 pair appears to encode a WD-repeats protein (Delichère et al, 1999) and SlX/Y4 a fructose-2, 6-bisphosphatase (Atanassov et al, 2001), and neither is likely to be involved in sex determination. The recombination fraction between SlX1 and SlX4 (Figure 2) suggests that they are far apart on the X, and potentially also on the Y chromosome, unless this has been rearranged. Comparisons of the coding sequences of these X-and Y-linked genes, including outgroup sequences in non-dioecious Silene species, yield Ka/Ks < 0.2 (Atanassov et al, 2001). The protein sequences of both the Y- and X-linked genes have therefore been maintained for at least most of their evolutionary history since the X and Y ceased recombining, ie these Y-linked genes have not degenerated. Silent site divergence between SlX4 and SlY4 is similar to that between the X- and Y-chromosome copies of MROS3, and both suggest an age estimate of the sex chromosome system similar to that based on the ITS sequences (Desfeux et al, 1996). The SlX1 and SlY1 genes are considerably less diverged. It will be very interesting to study more X/Y-linked gene pairs to test whether the Y chromosome seems to have been built up in a stepwise manner, as seems to be true of the human Y (Lahn and Page, 1999; Waters et al, 2001).
If the Y chromosomes of dioecious Silenes are actively degenerating, Y-linked genes are predicted to have reduced diversity, and we can use patterns of diversity at non-degenerated loci (such as those just described) to test for selective sweeps. In samples from several S. latifolia and S. dioica populations, SlY1 diversity is indeed lower than that of SlX1, after correcting for the smaller number of Y than X chromosomes in populations (Caballero, 1995). Analysis using outgroup sequences shows that this is not due to a higher mutation rate of the Y-linked genes (Filatov et al, 2001). Tests such as Tajima's test do not suggest selective sweeps (Filatov et al, 2000, 2001). However, these tests are affected by subdivision (Schierup et al, 2000), for which there is evidence in these species (McCauley, 1994; Giles et al, 1998; Ingvarsson and Giles, 1999; Richards et al, 1999), which probably affects the Y chromosome more than other chromosomes, because of its smaller effective size (Wang, 1999). Larger samples from within single populations are therefore needed. It is also difficult to test for diversity differences in the presence of introgression between the two Silene species. Y-chromosome variants differ between the two species, whereas some X-linked variants are shared between them (Filatov et al, 2001). A final difficulty is that autosomal loci are also needed in order to know whether Y-chromosomal variation is reduced, or X-linked diversity elevated. The one autosomal locus so far studied has low diversity, but this does not point to increased X-linked diversity, because this gene appears to have experienced a selective sweep (Filatov et al, 2001), so more autosomal genes are needed. Comparisons are also needed with species whose Y-chromosome is fully degenerated. If low diversity is also found in these, it would point to causes such as mutation rate differences, rather than effects of the selective processes during genetic degeneration.
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Discussion
With the availability of molecular techniques, we may now hope to understand more about how sex chromosomes evolve. Mapping data, even with anonymous markers, should give estimates of the fraction of X-linked loci that are located in the pairing and differential regions. In the absence of useful chromosome banding patterns that identify regions, single-copy anonymous markers can also be useful for mapping in combination with Y-chromosome deletions (Donnison et al, 1996). Deletion mapping of the Y chromosome does not precisely pinpoint the sex-determination loci, but it should be possible to define the regions in which these genes are located Figure 2 summarises current information about the S. latifolia Y.
Once genes have been identified and sequenced, we will be able to estimate how long sex chromosome evolution takes. This should help us evaluate the plausibility of the proposed mechanisms for the process. The results of such studies may, in turn, contribute to our knowledge of mutation rates to deleterious mutations, and to a growing body of understanding of evolution in the absence of recombination. Studies of the early stages of sex chromosome degeneration offer the potential to have a eukaryote version of the interesting results on genome degradation in asexual prokaryotes (Wernergreen and Moran, 1999). If, as appears likely, plant sex chromosomes are found to be only partially genetically degenerated, they may offer opportunities to help understand the relationship between the evolution of genetic degeneration and of dosage compensation.
To begin, you know I have not tested this idea, I stated this.
And because I never wrote or implied that CBN is produced by the plant directly I will not argue the case, even though you seem to want to fight about something. I implied that CBN is a product of THC degradation, as you so kindly retorted. This is why I referenced THC:CBD:CBN levels while posting about cannabinoid degradation.
Maybe I should have been more clear and posted about cannabigerolic acid, THC-COOH, decarboxylation, THC, and CBD... in that order with the required enzyme names where applicable and all the details. but you know all this stuff already.
From your homie (Marijuana Botany, An Advanced Study: The Propagation and Breeding of Distinctive Cannabis by Robert Connell Clarke.) sorry to everyone for my half-ass cite.
Hey, sorry for the agitated response. Let's clear this up as I am still slightly confused. Sorry to all for the off topic posts... but anything to distract from the 707 show "oh ya eh?" lol
I understand that you can increase CBN levels by exposing THC to heat/light/O2 post harvest. That is not the issue.
The issue is that I orginally said:
To which you responded:
You say cannabis plants do not produce CBN directly, that it is a degradation product of other cannabinoids, which are produced directly by the plant.
You also say that at the same time 'very very small amounts' of CBN CBN is found in most all cannabis plant matter.
The presence of CBN (even very very small amounts) in living cannabis plants may be from natural degradation of THC. Degradation that occurs while the plant is living.
SO with that all in mind... Why would letting plants over-ripen not affect CBN levels, or THC:CBD:CBN ratios? THC is degrading (be it small amounts or not) to CBN while the plants are living... correct?
I intentionally used the expression "to what degree I am unsure"...
Again I say I would like to read your info and couldn't find it??....Love to try your Skunk#2 but where is #1 ?..LOL .. Not sure if our Road kill skunk was yours but do tell where has she gone?peace out Headband707
