This has been debated, even tried. The last time i seen some one try it, they auto cutting didn't take. It just never perked up like the other non auto one did.
What i find interesting about the experiment, will the flowering be delayed at all by the size of the host plant. Could perhaps be an interesting side affect.
A theory that i feel explains what makes an auto auto, boils down to proteins building up that affect genes that can alter the circadian clock.
This one is for brick, since you are about the details mate. I didn't come up with all this, as i am not a geneticist. However you can determine what the message is. If you would like sources, i'll be happy to PM whom ever.
My hypnoses on the auto gene.
My hypnoses is
LHY late elongated hypocotyl gene
and/or
TOC1 Timing of CAB expression 1 gene
is responsible for flowering in Day-Neutral Cannabis, aka Auto-Flowering Cannabis.
I base this on the genetic (DNA mapping) work that has bend dun on Rosales.
The specie Cannabis is in the Cannabaceae family, which is in the order Rosales.
The dominant late elongated hypocotyl (lhy) disrupted circadian clock regulation of gene expression and leaf movements and caused flowering to occur independently of photoperiod. LHY was shown to encode a MYB DNA-binding protein. Increased LHY expression from a transgene caused the endogenous gene to be expressed at a constant level, suggesting that LHY was part of a feedback circuit that regulated its own expression. Thus, constant expression of LHY disrupts several distinct circadian rhythms and LHY may be closely associated with the central oscillator of the circadian clock. Of the central circadian clock genes, homologs of LHY and TOC1 were present in our EST libraries and GDR, respectively, but CCA1 was lacking from Rosaceae databases.
If you would like sources, i'll be happy to PM whom ever.
First, in response to your question of; "will the flowering be delayed at all by the size of the host plant?" I want to say no, other of course that the amount of time needed for the graft to take and heal and normal growth to then continue ... but that is pure assumption.
As for your sources, I would love to see all the sources you have, or at least links for them so PM away when you feel like doing so.
This is all beyond my level of plant knowledge and will take either a great deal of research or someone who is very educated in plant DNA and all facets of botany. The more you delve into it you find much more plays a part in the answer to the question than was stated in the initial question/theory message.
The central circadian clock genes, LHY and TOC1 are understandable and CCA1 was mentioned but without any real information of its functions or limits. When researched there appear to be limitations or things that can possibly control, partially control or at least somewhat alter it under certain conditions.
A hypocotyl, a dominant late elongated one or not, is the space between the radicle and the plumule. A hypocotyl develops into a stem. The radicle is the part of the embryo that emerges first and develops into a main root, root hairs and secondary roots. A plumule is like a leaf in its early development.
An elongated hypocotyl (lhy) encodes a MYB DNA-binding protein increasing LHY expression from a transgene, which is an exogenous gene introduced into the genome of another organism.
Research findings, though not performed on ruderalis or auto-flowering cannabis or any genus cannabis, and instead on other non-photoperiod plants found that transcriptional feedback loops constitute the molecular circuitry of the plant circadian clock and there is a core loop is established between CCA1 and TOC1.
Transcriptional feedback loops constitute the molecular circuitry of the plant circadian clock. A core loop is established between CCA1 and TOC1. Although CCA1 directly represses TOC1, the TOC1 protein has no DNA binding domains, which suggests that it cannot directly regulate CCA1. A functional genomic established strategy that led to the identification of CHE, a TCP transcription factor that binds specifically to the CCA1 promoter. CHE is a clock component partially redundant with LHY in the repression of CCA1. The expression of CHE is regulated by CCA1, thus adding a CCA1/CHE feedback loop to the circadian network. Because CHE and TOC1 interact, and CHE binds to the CCA1 promoter, a molecular linkage between TOC1 and CCA1 gene regulation is established
Now you have TOC1 protein and CHE thrown into the mix that were not initially mentioned, though might be in your sources.
For me to be able to answer the question correctly it will take a lot of time and a lot of serious research, so for my sake I hope your sources hold the answers or there is someone here who is in expert in plant DNA and plant functions that can give a simple answer because certain things appear to be contradictory to me and others just incredibly difficult to understand since I do not understand everything about the topic.
