Fleshing this out a bit more: insofar as development is synchronized in an organism, there usually has to be some high-level signal to trigger the synchronized transitions. Given the scale over which the signal needs to apply (i.e. across the whole brain in this case), it probably has to be one or a few small molecules which diffuse in the extracellular space. As I’m looking into possibilities here, one of my main threads is to look into both general and brain-specific developmental signal molecules in human childhood, to find candidates for the relevant molecular signals.
(One major alternative model I’m currently tracking is that the brain grows to fill the brain vault, and then stops growing. That could in-principle mechanistically work via cells picking up on local physical forces, rather than a small molecule signal. Though I don’t think that’s the most likely possibility, it would be convenient, since it would mean that just expanding the skull could induce basically-normal new brain growth by itself.)
I hope by now you’re already familiar with michael levin & his lab’s work on the subject of morphogenesis signals? Pretty much everything I’m thinking here is based on that.
Yes, it’s absolutely a combination of chemical signals and physical pressure. An interesting specific example of these two signals working together during fetal development when the pre-neurons are growing their axons. There is both chemotaxis which steers the ameoba-like tip of the growing axon, and at the same time a substantial stretching force along the length of the axon. The stretching happens because the cells in-between the origin and current location of the axon tip are dividing and expanding. The long distance axons in the brain start their growth relatively early on in fetal development when the brain is quite small, and have gotten stretched quite a lot by the time the brain is near to birth size.
Fleshing this out a bit more: insofar as development is synchronized in an organism, there usually has to be some high-level signal to trigger the synchronized transitions. Given the scale over which the signal needs to apply (i.e. across the whole brain in this case), it probably has to be one or a few small molecules which diffuse in the extracellular space. As I’m looking into possibilities here, one of my main threads is to look into both general and brain-specific developmental signal molecules in human childhood, to find candidates for the relevant molecular signals.
(One major alternative model I’m currently tracking is that the brain grows to fill the brain vault, and then stops growing. That could in-principle mechanistically work via cells picking up on local physical forces, rather than a small molecule signal. Though I don’t think that’s the most likely possibility, it would be convenient, since it would mean that just expanding the skull could induce basically-normal new brain growth by itself.)
I hope by now you’re already familiar with michael levin & his lab’s work on the subject of morphogenesis signals? Pretty much everything I’m thinking here is based on that.
Yes, I am familiar with Levin’s work.
Yes, it’s absolutely a combination of chemical signals and physical pressure. An interesting specific example of these two signals working together during fetal development when the pre-neurons are growing their axons. There is both chemotaxis which steers the ameoba-like tip of the growing axon, and at the same time a substantial stretching force along the length of the axon. The stretching happens because the cells in-between the origin and current location of the axon tip are dividing and expanding. The long distance axons in the brain start their growth relatively early on in fetal development when the brain is quite small, and have gotten stretched quite a lot by the time the brain is near to birth size.