MAST1: MACROSCOPIC LOCAL PERTURBATIONS IN BRAIN GROWTH

 

 
My electronic response to an intriguing paper publised by Neuron
 
 
 
 
 
 
In this paper, Tripathy et al. (2018) report that Mast1, espressed just in postmitotic neuronal dendritic and axonal compartments, is associated with the microtubule cytoskeleton in a MAP-dependent manner. Mice with Mast1 microdeletions display peculiar macroscopic features, such as enlarged corpus callosum and smaller cerebellum, in absence of megalencephaly. These opposite findings (abnormal increase vs abnormal reduction) let us to hypothesize that the macroscopic growth of the brain tissue is regulated by physical constrains: keeping invariant the brain size (i.e., in absence of megaloencephaly), the central nervous tissue of animals harboring Mast1 microdeletions undergoes a general rearrangement. In physical/mathematical terms, a three-dimensional lattice (standing for the whole brain mass) harbors vectors and tensors which product must be held constant. When a lattice perturbation occurs (as in the case of cytoskeleton genetic Mast1 alterations), one of the tensors modifies. In order to keep invariant the tensor product, another tensor need to vary: in simpler words, the fact that more axons cross the midline in Mast1 Leu278 del mice means that the size of other structures (in this case, the cerebellum) must decrease. In touch with this observation, Tripathy et al. (2018) report that, in animals harboring Mast1 microdeletions, we find the PI3K/AKT3/mTOR pathway unperturbed, whereas Mast2 and Mast3 levels are diminished, indicative of a dominant-negative mode of action.
 
 
 
Read more: https://arturotozzi.webnode.it/products/mast1-macroscopic-local-perturbations-in-brain-growth/
 
 
 
 
 
 
In this paper, Tripathy et al. (2018) report that Mast1, espressed just in postmitotic neuronal dendritic and axonal compartments, is associated with the microtubule cytoskeleton in a MAP-dependent manner. Mice with Mast1 microdeletions display peculiar macroscopic features, such as enlarged corpus callosum and smaller cerebellum, in absence of megalencephaly. These opposite findings (abnormal increase vs abnormal reduction) let us to hypothesize that the macroscopic growth of the brain tissue is regulated by physical constrains: keeping invariant the brain size (i.e., in absence of megaloencephaly), the central nervous tissue of animals harboring Mast1 microdeletions undergoes a general rearrangement. In physical/mathematical terms, a three-dimensional lattice (standing for the whole brain mass) harbors vectors and tensors which product must be held constant. When a lattice perturbation occurs (as in the case of cytoskeleton genetic Mast1 alterations), one of the tensors modifies. In order to keep invariant the tensor product, another tensor need to vary: in simpler words, the fact that more axons cross the midline in Mast1 Leu278 del mice means that the size of other structures (in this case, the cerebellum) must decrease. In touch with this observation, Tripathy et al. (2018) report that, in animals harboring Mast1 microdeletions, we find the PI3K/AKT3/mTOR pathway unperturbed, whereas Mast2 and Mast3 levels are diminished, indicative of a dominant-negative mode of action.