XB-ART-54051Dev Dyn January 1, 2018; 247 (1): 124-137.
Asymmetric development of the nervous system.
The human nervous system consists of seemingly symmetric left and right halves. However, closer observation of the brain reveals anatomical and functional lateralization. Defects in brain asymmetry correlate with several neurological disorders, yet our understanding of the mechanisms used to establish lateralization in the human central nervous system is extremely limited. Here, we review left-right asymmetries within the nervous system of humans and several model organisms, including rodents, Zebrafish, chickens, Xenopus, Drosophila, and the nematode Caenorhabditis elegans. Comparing and contrasting mechanisms used to develop left-right asymmetry in the nervous system can provide insight into how the human brain is lateralized. Developmental Dynamics 247:124-137, 2018. © 2017 Wiley Periodicals, Inc.
PubMed ID: 28940676
PMC ID: PMC5743440
Article link: Dev Dyn
Genes referenced: arse lhb nodal notch1
GO Terms: brain development
Article Images: [+] show captions
|Figure 1. Laterality in the human nervous system. The left and right hemispheres of the human brain are connected by the corpus callosum. The hemispheres display functional differences and control contralateral sides of the human body. Broca's and Wernicke's areas are language centers located in the left hemisphere of the majority of individuals. A, anterior; L, left; P, posterior; R, right.|
|Figure 2. Lateralization of the nervous system in Zebrafish and chicken. A: Asymmetry of the epithalamus and lateralization of eye use in Zebrafish. Nodal from the lateral plate mesoderm induces its own expression in the left habenula. FGF and Nodal act together to ensure directional asymmetry of the epithalamus. B: Lateralization of eye use in chicken. A, anterior; Hb, habenula; L, left; LHb, lateral habenula (green); LPM, lateral plate mesoderm; MHb, medial habenula (blue); P, posterior; Po, pineal organ (purple); Pp, parapineal organ (purple); R, right.|
|Figure 4. Establishment of directional ASE asymmetry in C. elegans. Priming and boosting of lsy-6 miRNA throughout the ASEL cell lineage leads to the ASEL identity. At the 4-cell stage, activated Notch receptor in the ASER precursor inhibits priming and boosting events of lsy-6 miRNA, leading to the ASER identity. TF, transcription factor; purple, active ASER-promoting molecules; blue, active ASEL-promoting molecules; grey, less active or inactive molecules; circles represent cells.|