"All of the tissues and organs of the body arise from one of three embryonic precursors: the ectoderm, mesoderm and endoderm. The ectoderm contributes to several tissues, including the nervous system and the skin, but some studies have suggested that development into neurons requires nothing more than the absence of specific inhibitory signals."Terminally interested as I am in unfoldment of the HumanAntiGravitySuit, I took a closer look and saw this, next:
"This phenomenon has led biologists to formulate what is called the ‘neural default model’. “The simplest interpretation of the neural default model is that the neural fate is a ‘left-over’ choice, passively determined by the elimination of other pathways of differentiation,” explains Yoshiki Sasai of the RIKEN Center for Developmental Biology in Kobe."So, I wonder, is the 'neural default mode' to the embryo similar to the situation of the female gender (in humans at least) as 'default' human phenotype, requiring all sorts of special chomosomal, hormonal and anatomical applications to build the alternate, i.e. males? Or all those interesting XXY's and XYY's etc., inbetweeners? not to mention all the other aneuploidic people?
But really, this is a stray thought.
Further along in the story, whoever-the-author-is points out that calling something a 'default mode' doesn't contribute any explanation about what drives the nervous system to develop. Clever researchers are investigating that very topic. Right down to a single protein, Zfp521:
"They identified one intriguing candidate, Zfp521, which activated several other genes involved in neural development, even when the mES cells were cultured in the presence of factors that would normally curb this process."So, it's ever more interesting even as I feel the water of scientific minutia closing over my head and drowning me for the kajillionth time. Good thing I can still breathe under that kind of water. I generally figure, the more I can expose my creaky brain to information, the more likely it will finally be able to retain some of it. Just a hunch, but this strategy usually has worked for me in the past.
Anyway, some links to some pretty heavy papers were included at the end of the story, which is always appreciated.. not that they always are decipherable by me in the moment:
1. Kamiya, D., et al. Intrinsic transition of embryonic stem-cell differentiation into neural progenitors. Nature 470, 503–509 (2011).
2. Watanabe, K., et al. Directed differentiation of telencephalic precursors from embryonic stem cells. Nature Neuroscience 8, 288–296 (2005).
From the link to the second paper, I strayed to a link that went to this:
Amygdala and neocortex: common origins and shared mechanisms (Ooh, that sounds kinda juicy...) which discusses an article, A stream of cells migrating from the caudal telencephalon reveals a link between the amygdala and neocortex.
Fills in a bit of the story about how the amygdala arrives first on the scene, before the neocortex, evolutionarily, developmentally and functionally, then becomes a very fast and very bossy little spy, gathering the first scoop on any situation and always, throughout the whole lifespan, tries to tell the neocortex how to feel and think.
ABSTRACT: The amygdaloid complex consists of diverse nuclei that belong to distinct functional systems, yet many issues about its development are poorly understood. Here, we identify a stream of migrating cells that form specific amygdaloid nuclei in mice. In utero electroporation showed that this caudal amygdaloid stream (CAS) originated in a unique domain at the caudal telencephalic pole that is contiguous with the dorsal pallium, which was previously thought to generate only neocortical cells. The CAS and the neocortex share mechanisms for specification (transcription factors Tbr1, Lhx2 and Emx1/2) and migration (reelin and Cdk5). Reelin, a critical cue for migration in the neocortex, and Cdk5, which is specifically required for migration along radial glia in the neocortex, were both selectively required for the normal migration of the CAS, but not for that of other amygdaloid nuclei. This is first evidence of a dorsal pallial contribution to the amygdala, demonstrating a developmental and mechanistic link between the amygdala and the neocortex.