Lineage-specific requirements of β-catenin in neural crest development

β-Catenin plays a pivotal role in cadherin-mediated cell adhesion. Moreover, it is a downstream signaling component of Wnt that controls multiple developmental processes such as cell proliferation, apoptosis, and fate decisions. To study the role of β-catenin in neural crest development, we used the Cre/loxP system to ablate β-catenin specifically in neural crest stem cells. Although several neural crest–derived structures develop normally, mutant animals lack melanocytes and dorsal root ganglia (DRG). In vivo and in vitro analyses revealed that mutant neural crest cells emigrate but fail to generate an early wave of sensory neurogenesis that is normally marked by the transcription factor neurogenin (ngn) 2. This indicates a role of β-catenin in premigratory or early migratory neural crest and points to heterogeneity of neural crest cells at the earliest stages of crest development. In addition, migratory neural crest cells lateral to the neural tube do not aggregate to form DRG and are unable to produce a later wave of sensory neurogenesis usually marked by the transcription factor ngn1. We propose that the requirement of β-catenin for the specification of melanocytes and sensory neuronal lineages reflects roles of β-catenin both in Wnt signaling and in mediating cell–cell interactions

The molecular machinery of myelin gene transcription in Schwann cells

During late fetal life, Schwann cells in the peripheral nerves, singled out by the larger axons will transit through a promyelinating stage before exiting the cell cycle and initiating myelin formation. A network of extra- and intracellular signaling pathways, regulating a transcriptional program of cell differentiation, governs this progression of cellular changes, culminating in a highly differentiated cell. In this review we focus on the roles of a number of transcription factors not only in myelination, during normal development, but also in demyelination, following nerve trauma. These factors include specification factors involved in early development of Schwann cells from neural crest (Sox10) as well as factors specifically required for transitions into the promyelinating and myelinating stages (Oct6/Scip and Krox20/Egr2). From this description we can glean the first, still very incomplete, contours of a gene regulatory network that governs myelination and demyelination during development and regeneration

pyiron/pylammpsmpi: pylammpsmpi 0.2.7

<h2>What's Changed</h2> <ul> <li>Update black action by @jan-janssen in https://github.com/pyiron/pylammpsmpi/pull/160</li> <li>Bump scipy from 1.11.3 to 1.11.4 by @dependabot in https://github.com/pyiron/pylammpsmpi/pull/158</li> <li>Bump numpy from 1.26.0 to 1.26.2 by @dependabot in https://github.com/pyiron/pylammpsmpi/pull/155</li> <li>Test lower limits of dependencies by @jan-janssen in https://github.com/pyiron/pylammpsmpi/pull/159</li> <li>Switch to pyproject.toml by @jan-janssen in https://github.com/pyiron/pylammpsmpi/pull/161</li> </ul> <p><strong>Full Changelog</strong>: https://github.com/pyiron/pylammpsmpi/compare/pylammpsmpi-0.2.6...pylammpsmpi-0.2.7</p&gt

pyiron/pylammpsmpi: pylammpsmpi 0.2.5

<h2>What's Changed</h2> <ul> <li>Update pympipool to 0.7.1 by @jan-janssen in https://github.com/pyiron/pylammpsmpi/pull/146</li> <li>Use Coveralls Github action by @jan-janssen in https://github.com/pyiron/pylammpsmpi/pull/147</li> <li>Update Lammps to 2023.08.02 by @jan-janssen in https://github.com/pyiron/pylammpsmpi/pull/148</li> <li>Bump mpi4py from 3.1.4 to 3.1.5 by @dependabot in https://github.com/pyiron/pylammpsmpi/pull/150</li> <li>Bump pympipool from 0.7.1 to 0.7.2 by @dependabot in https://github.com/pyiron/pylammpsmpi/pull/153</li> </ul> <p><strong>Full Changelog</strong>: https://github.com/pyiron/pylammpsmpi/compare/pylammpsmpi-0.2.4...pylammpsmpi-0.2.5</p&gt

pyiron/pylammpsmpi: pylammpsmpi 0.2.6

<h2>What's Changed</h2> <ul> <li>Bump pympipool from 0.7.2 to 0.7.3 by @dependabot in https://github.com/pyiron/pylammpsmpi/pull/154</li> <li>Use trusted publisher action by @jan-janssen in https://github.com/pyiron/pylammpsmpi/pull/156</li> <li>Update pympipool to 0.7.5 by @jan-janssen in https://github.com/pyiron/pylammpsmpi/pull/157</li> </ul> <p><strong>Full Changelog</strong>: https://github.com/pyiron/pylammpsmpi/compare/pylammpsmpi-0.2.5...pylammpsmpi-0.2.6</p&gt

Expression of truncated PrP targeted to Purkinje cells of PrP knockout mice causes Purkinje cell death and ataxia

PrP knockout mice with disruption of only the PrP-encoding region (Zürich I-type) remain healthy, whereas mice with deletions extending upstream of the PrP-encoding exon (Nagasaki-type) suffer Purkinje cell loss and ataxia, associated with ectopic expression of Doppel in brain, particularly in Purkinje cells. The phenotype is abrogated by co-expression of full-length PrP. Doppel is 25% similar to PrP, has the same globular fold, but lacks the flexible N-terminal tail. We now show that in Zürich I-type PrP-null mice, expression of N-terminally truncated PrP targeted to Purkinje cells also leads to Purkinje cell loss and ataxia, which are reversed by PrP. Doppel and truncated PrP probably cause Purkinje cell degeneration by the same mechanism