Summary of the presentation
During the course of vertebrate evolution thyroid hormone acquired multiple roles in development, especially brain development. Examples of thyroid action on nervous system development include promotion of myelination, thereby increasing speed of neuronal transmission, as well as modulation of neuronal differentiation, as exemplified by the exquisite sensitivity of the Purkinje neuron to thyroid hormone deficiency, or the determination of neuronal versus glial fates by changes in thyroid hormone availability. Differing ratios of neuron to glia numbers have also been implicated in evolution of the primate brain [2, 3]. Our current work is addressing the question of how thyroid hormone signalling plays a role in glial lineage and oligodendrocyte determination. Overall the effect of active thyroid hormone signalling appears to be commitment of progenitors to the neuronal lineage. Differential control of brain progenitor pool size and lineage decisions has been suggested as a driver in evolution of the primate and human brain. Putting our results on thyroid hormone control of progenitor lineage decision and progenitor commitments adds another perspective to the co-evolution of thyroid hormone signalling and the process of cephalisation in vertebrates. A final point that will be discussed is that these regulatory processes could be prime targets of endocrine disruption.
1. Lopez-Juarez, A., et al., Thyroid hormone signaling acts as a neurogenic switch by repressing Sox2 in the adult neural stem cell niche. Cell Stem Cell, 2012. 10(5): p. 531-43.
2. Herculano-Houzel, S., The glia/neuron ratio: how it varies uniformly across brain structures and species and what that means for brain physiology and evolution. Glia, 2014. 62(9): p. 1377-91.
3. Sherwood, C.C. et al., Evolution of increased glia-neuron ratios in the human frontal cortex. Proc Natl Acad Sci U S A, 2006. 103(37): p. 13606-11.
4. Miller, J.A. et al., Transcriptional landscape of the prenatal human brain. Nature, 2014. 508(7495): p. 199-206.
Brain, evolution, endocrine