In DRG11 knockout mice, trigeminal cell death is extensive and does not account for failed brainstem patterning
| Autor: | Charles E. Ribak, Zhou-Feng Chen, Joop J.A. Arends, Mark F. Jacquin, Lee A. Shapiro, Chuanxi Xiang |
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| Jazyk: | angličtina |
| Rok vydání: | 2008 |
| Předmět: |
Programmed cell death
Pathology medicine.medical_specialty Necrosis animal diseases viruses Cell Count Nerve Tissue Proteins Biology Trigeminal Nuclei Article Mice Bcl-2-associated X protein Microscopy Electron Transmission medicine Animals Body Patterning Cell Size bcl-2-Associated X Protein Homeodomain Proteins Mice Knockout Neurons Afferent Pathways Analysis of Variance Cell Death General Neuroscience Embryo Mammalian Molecular biology Ganglion medicine.anatomical_structure Animals Newborn Apoptosis Vibrissae Knockout mouse biology.protein Brainstem medicine.symptom Nucleus Brain Stem Transcription Factors |
| Popis: | A previous study (Ding et al., 2003) showed that the homeodomain transcription factorDRG11is necessary for pattern formation in the trigeminal nucleus principalis (PrV), the requisite brainstem nucleus for development of the whisker-to-barrel cortex pathway. However, it is not known howDRG11contributes to pattern formation. Anatomical studies were performed inDRG11knock-out (−/−) andDRG11/Baxdouble −/− mice to test the hypotheses thatDRG11is required for neuronal survival in the V pathway and that PrV cell death is sufficient to explain pattern alterations. At birth,DRG11−/−mice had equivalent cell loss in the V ganglion, PrV, and spinal V subnucleus interpolaris (SpVi). Because whisker-related patterns were normal in the SpVi, cell death would not appear to explain failed pattern formation in the mutant PrV. Electron microscopy revealed exuberant apoptosis and necrosis as the mechanisms of PrV cell death occurring in the late prenatal and newbornDRG11−/−, when such cell death was up to six times more prevalent than normal.DRG11heterozygote andBax−/−mice were crossed in an attempt to dissociate PrV patterning anomalies from exuberant apoptosis inDRG11−/−mice. BothDRG11−/−andDRG11/Baxdouble −/− mutants lacked whisker-related patterning in their PrV, despiteBax−/−-induced rescue of V ganglion and PrV cells. Thus, apoptotic cell death is not a sufficient cause of failed pattern formation in the PrV of theDRG11−/−. A signaling pathway involvingDRG11may, therefore, be the elusive PrV pattern maker. |
| Databáze: | OpenAIRE |
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