Back

Fetal neural progenitors process TLR signals from bacterial components to enhance proliferation and rework brain development

Mann, B.; Crawford, J. C.; Reddy, K.; Lott, J.; Youn, Y. H.; Gao, G.; Guy, C.; Chou, C.-h.; Darnell, D.; Trivedi, S.; Bomme, P.; Loughran, A. J.; Thomas, P.; Han, Y.-G.; Tuomanen, E.

2021-10-19 neuroscience
10.1101/2021.10.19.464985 bioRxiv
Show abstract

Bacterial cell wall, a universal pathogen-associated molecular pattern (PAMP), crosses the placenta into the fetal brain. We determined that PAMPs interact with TLR2/6 on murine fetal neural progenitor cells (NPCs) to induce overexpansion of all neocortical layers leading to a larger, folded cortex and abnormal postnatal behavior. The NPC overexpansion originated at E10 and targeted ventricular radial glia (vRG), the primary NPC, by shortening cell cycle and increasing self-renewal. The mechanism involved two novel signaling pathways in NPCs mediated by recognition of bacterial PAMPs by TLR2/6 including: a) loss of primary cilia, activation of hedgehog signaling, and increased FOXG1 and b) increased PI3K/AKT activity. These findings reveal PAMP/TLR2/6 acts as a morphogen in fetal neurodevelopment. In addition, the loss of Tlr2 or Tlr6 without pathogenic challenge, increased the number of neurons, establishing the requirement for an endogenous TLR2 signal for normal neurodevelopment in the embryo.

Matching journals

The top 3 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.