Mutation of the BiP/GRP78 gene causes axon outgrowth and fasciculation defects in the thalamocortical connections of the mammalian forebrain

التفاصيل البيبلوغرافية
العنوان: Mutation of the BiP/GRP78 gene causes axon outgrowth and fasciculation defects in the thalamocortical connections of the mammalian forebrain
المؤلفون: Cynthia M. Grimsley-Myers, Noelle D. Dwyer, Ayushma Shrestha, David R. Beier, Carlita B. Favero, Rasha N. Henshaw
المصدر: Journal of Comparative Neurology. 521:677-696
بيانات النشر: Wiley, 2012.
سنة النشر: 2012
مصطلحات موضوعية: Male, Mutant, Gestational Age, Biology, Article, Mice, Mice, Neurologic Mutants, Prosencephalon, Thalamus, Pregnancy, Neural Pathways, medicine, Animals, Genetic Testing, Axon, Endoplasmic Reticulum Chaperone BiP, Cells, Cultured, Heat-Shock Proteins, Cerebral Cortex, Mammals, Cerebrum, General Neuroscience, Endoplasmic reticulum, Axon extension, Fibroblasts, Axons, Mice, Inbred C57BL, medicine.anatomical_structure, nervous system, Forebrain, Female, Axon guidance, Neuroscience, Genetic screen
الوصف: Proper development of axonal connections is essential for brain function. A forward genetic screen for mice with defects in thalamocortical development previously isolated a mutant called baffled. Here we describe the axonal defects of baffled in further detail and identify a point mutation in the Hspa5 gene, encoding the endoplasmic reticulum chaperone BiP/GRP78. This hypomorphic mutation of BiP disrupts proper development of the thalamocortical axon projection and other forebrain axon tracts, as well as cortical lamination. In baffled mutant brains, a reduced number of thalamic axons innervate the cortex by the time of birth. Thalamocortical and corticothalamic axons are delayed, overfasciculated, and disorganized along their pathway through the ventral telencephalon. Furthermore, dissociated mutant neurons show reduced axon extension in vitro. Together, these findings demonstrate a sensitive requirement for the endoplasmic reticulum chaperone BiP/GRP78 during axon outgrowth and pathfinding in the developing mammalian brain. J. Comp. Neurol. 521:677–696, 2013. © 2012 Wiley Priodcals, Inc.
تدمد: 0021-9967
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dd7381424e4459fb237caf4a62caef53Test
https://doi.org/10.1002/cne.23199Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....dd7381424e4459fb237caf4a62caef53
قاعدة البيانات: OpenAIRE