ArticleNeural development2015
Pax6 is required intrinsically by thalamic progenitors for the normal molecular patterning of thalamic neurons but not the growth and guidance of their axons.
Article in Neural development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 14 citations in OpenAlex.
- Sensory modality-specific wiring of thalamocortical circuits.Nature reviews. Neuroscience · 2025Review
- Development of the early fetal human thalamus: from a protomap to emergent thalamic nuclei.Frontiers in neuroanatomy · 2025Article
- Generation of ventralized human thalamic organoids with thalamic reticular nucleus.Cell stem cell · 2023Article
- Article
- The role of the diencephalon in the guidance of thalamocortical axons in mice.Development (Cambridge, England) · 2020Article
- Pax6 organizes the anterior eye segment by guiding two distinct neural crest waves.PLoS genetics · 2020Article
- Comparison of two related lines of tauGFP transgenic mice designed for lineage tracing.BMC developmental biology · 2017Article
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6 authors at 2 institutions in 2 countries.
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Abstract
backgroundIn mouse embryos, the Pax6 transcription factor is expressed in the progenitors of thalamic neurons but not in thalamic neurons themselves. Its null-mutation causes early mis-patterning of thalamic progenitors. It is known that thalamic neurons generated by Pax6 (-/-) progenitors do not develop their normal connections with the cortex, but it is not clear why. We investigated the extent to which defects intrinsic to the thalamus are responsible.
resultsWe first confirmed that, in constitutive Pax6 (-/-) mutants, the axons of thalamic neurons fail to enter the telencephalon and, instead, many of them take an abnormal path to the hypothalamus, whose expression of Slits would normally repel them. We found that thalamic neurons show reduced expression of the Slit receptor Robo2 in Pax6 (-/-) mutants, which might enhance the ability of their axons to enter the hypothalamus. Remarkably, however, in chimeras comprising a mixture of Pax6 (-/-) and Pax6 (+/+) cells, Pax6 (-/-) thalamic neurons are able to generate axons that exit the diencephalon, take normal trajectories through the telencephalon and avoid the hypothalamus. This occurs despite abnormalities in their molecular patterning (they express Nkx2.2, unlike normal thalamic neurons) and their reduced expression of Robo2. In conditional mutants, acute deletion of Pax6 from the forebrain at the time when thalamic axons are starting to grow does not prevent the development of the thalamocortical tract, suggesting that earlier extra-thalamic patterning and /or morphological defects are the main cause of thalamocortical tract failure in Pax6 (-/-) constitutive mutants.
conclusionsOur results indicate that Pax6 is required by thalamic progenitors for the normal molecular patterning of the thalamic neurons that they generate but thalamic neurons do not need normal Pax6-dependent patterning to become competent to grow axons that can be guided appropriately.
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