Interorgan Signals

June 4, 2015 For simplicity focusing on big six: Lungs, heart, kidneys, liver, stomach and  intestines ( large and small). Given that the brain sends and receives chemical and electrical signals from all organs, sensory and others.

Do the lungs communicate with the kidneys in any way? Does the heart communicate with the liver? The stomach with the lungs?

Rather than hierarchical communication centered on the brain, a rhizomatic system between all organs in constant, precise communication.

How does stomach tissue signal the heart-lungs that it is dying from lack of oxygen?

Does lung disease cause oxygen deprivation problems in all organ systems? what happens when the blood cannot carry enough oxygen for ATP production and all cells become energy-starved?

Does oxygen deprivation accelerate cancer onset and growth?

Miscellaneous Questions:

  1. RNA codes for some proteins that return to act upon the genome itself - the originating DNA molecules. Does this mean that a protein re-enters the cell nucleus from its point of production on a ribosome at nucleus-encircling rough endoplasmic reticulum. Is this protein assembled within the cell nucleus from ribosomes that did not migrate from their zone of origin at nucleolus out to the rough endoplasmic reticulum or is there rough endoplasmic reticulum within the nucleus?
  2. Are all 20 amino acids present in every cell type? One would think that only those amino acids required for a particular cell type’s proteinic product.
  3. Are amino acids imported into cells or created from scratch within each cell?
  4. Oneiric question: How many different brain areas must our dream machine tap into in order to create those scenes in places we have never been, populated by people we have never seen, with buildings of a type never imagined, living through social roles never experienced? Is this dream-stuff located in a long-term memory zone of the hippocampus,  mixing and matching from previous experience to create a unique movie? Must some dream nucleus reach out with its dendritic rhizomatic web into various sensory regions of the neocortex for every sight, smell, sound, color, face, weather condition, assembling these into a coherent though still mysterious story.
  5. Might prehistoric DNA have cannibalized itself to create an origin event for a new kingdom, phylum, class, order, family, genus or species? Say an ancient organism one billion years ago  had only one chromosome with 100 million base pairs. 80,000 base pairs of these 100 million split down their center i.e. unzip,  break off from main strand and end up ejected from this cell as two strands of RNA and then excreted by  the organism itself. Extracellular environment is such that this nuclear material can float freely, remaining intact and multiplying.

Hapleate, hapleated, hapleation, haplioid: A JB neologism that means to remove 23 of 46 chromosomes of any somatic cell from any organ in order to create a new haploid cell that is not a germ cell.

  1. Experiment One: Insert 23 chromosomes from a colon cell into a hapleated kidney cell nucleus. adjust each of these haplioids prior to insertion through post translational modifications so that they are pluripotent
  2. Insert hapleated kidney cell chromosomes into hapleated stomach cell nucleus. Has a viable zygote has been created?
  3. Experiment Two: Variation on #6 Knock out various combinations of regulatory accessory DNA in hippocampal neuron, hapleate, merge with hapleated liver cell nucleus to create Neo-germ cells
  4. Experiment Three: Relocate half of mouse neocortex to a zone just below the cerebellum of target mouse - see if new neuronal connections are made thus increasing brain power of target mouse. Is target mouse smarter after six months of synaptic growth?
  5. Experiment Four: Relocate neocortical mouse-one neurons into thalamic ventricle of same mouse - see if these neocortical neurons add value to hippocampal function.  Mix and match various brain cell types into different brain areas to see if brain cells can be re-purposed.
  6. Experiment Five:  Plant a slab of neocortex of healthy, young recently deceased ape,Party One, across the lower back of a healthy living ape, Party Two- - initiate axonal links from relocated ape neocortex into spinal cord of of Party Two - see if this transplanted neocortex has added consciousness to Party Two. Try neocortical transplant at various regions closer to the head, say at back of neck. try this on rats, mice, other primates, dogs, cats etc. Has any memory from Ape One been transmitted to Ape Two? A maze pattern or Pavlovian response unique to Ape One into Ape Two?
  7. Experiment Six: Replace cerebrospinal fluid at lateral ventricle(s) with new neuron population. Check for increased caudate nucleus or hippocampus function. Perform this neuron relocation to 3d, 4th ventricles with specific neuron types involved in specific signalling or hormonal process.
  8. Experiment Seven: Transplant brain cells from the pons or medulla to the lateral ventricles. Attach axons to any deficient brain area injured in battle or accident or genetic mishap. Whichever brain area is deficient could receive 200,000 additional neurons / brain cells to assist in restoration of brain function.
  9. Experiment Seven-A: Switch on or off specific DNA regions at these relocated    ( new) brain cells in order to customize function for specific tasks.
  10. Must any or all interorgan signaling travel through the brainstem like afferent-efferent signal from sensory organ to and from brain?
  11. Is interorgan signaling reflexive bypassing brain and even perhaps the spinal cord - direct organ to organ signal.

The following is a letter to Cal Tech Professor Elliot Meyerowitz re: interorgan signaling in a tree:

Dear Professor Meyerowitz,

I encountered a brief description of your work on structural forces effects upon patterns of plant growth while reading an article about Professor Jennifer Zallen and mechanical forces on Drosophila embryo growth.

I have wondered lately about the large scale growth of primary branches of an 60 foot tall oak tree in my rear yard (6 acre farmette in Lebanon, TN). I was trained as an architect at the Harvard GSD where I was introduced to D'Arcy Thompson so was primed to think about such things.  My questions are as follows:

  1. How does a big tree signal the amount of new growth in order to maintain its structural equilibrium? The compressive and tensile forces can be very large in a big tree under equilibrium ( compression) and tension resulting from regular lateral forces of wind and traumatic force induced after losing a major branch during lightning strike or pruning.
  1. Say a big branch on the left side of this big oak got blasted off by lightning one night;  the tree would have a lot of new compressive force in the cells on the side opposite the loss and lots of new tensile force in the cells on the side that lost the big branch.
  1.  My question: Is it the strain ( deformation measurable via strain gauge - a common structural engineering tool) of the compression force or the strain of the tensile force that initiates compensating new growth thus ensuring the balance of the entire tree in its new configuration? new growth that may be initiated by pathways you describe for Arabidopsis growth patterns i.e. PIN1 - Auxin or Ms Zallen's myosin-actin(cell adhesion under tension) biochemical process.
  1. Whatever these forces are at work on the large deformed tree, they must be similar for a plant sensing tensile or compressive forces in its hierarchy of stems as it grows from seed to maturity.
  1. I wonder if different chemical pathways are involved in compressive strain as opposed to those at work under tension forces. Each side of a plant having its own chemistry depending on tension or compression stress OR one side of a big tree ( or small plant) sending signals from one side to the other.

I'm using basic statics- architectural-structural engineering definitions for stress ( pounds per square inch, or whatever units force divided by area) and strain  (deformation in inches, fractions thereof)  in relation to tensile force.

  1. It would be interesting to measure relative amounts of PIN1 and auxin before and after an amputation of a large tree limb to investigate chemical changes.

Good luck in your researches

Warm Regards,

Jim Blake -Harvard GSD '79

Reply: Dear Mr. Blake,

All very good questions.  To the degree that we have answers, you can read them in the Wikipedia article on reaction wood (  We don’t know the signaling mechanism that leads to this adaptation to stress (or strain) - initially something must strain (a protein molecule, a membrane, who knows) and it is thought that auxin is involved, so PIN proteins probably are part of the mechanism.  The response depends on the type of tree - tension wood at the top of the branch in angiosperms, compression wood at the bottom in gymnosperms - but as far as I know, no one has the least idea why.

Just one more area open for research!

It is surprising sometime how little we know about plants, given their importance to us, but as you know our federal science agencies are very much slanted toward animal research in service of medicine, and in applied, not basic, plant studies.  The good part of this is that plenty of interesting phenomena are barely studied, so are open for new investigation.  The bad part is that there aren’t a lot of resources for such investigations, or many available answers to even simple questions about plants.

One area my lab studies (and not mentioned in the article), in a similar vein, is grafting in plants - no one knows why it works (or fails when it doesn’t work), despite large parts of agriculture relying in it.  I enclose a recent review and a research paper, in case you are interested.

Elliot Meyerowitz

Elliot M. Meyerowitz

George W. Beadle Professor of Biology

HHMI-GBMF Investigator

Division of Biology and Biological Engineering

Mail Code 156-29

California Institute of Technology

1200 East California Boulevard

Pasadena, California 91125, USA

  • 6/4/15