Please use this identifier to cite or link to this item:
http://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/3095
Title: | Role of FMN2 in Axonal Branching |
Authors: | GHOSE, AURNAB DAS, SOORAJ Dept. of Biology 20141080 |
Keywords: | 2019 Neurobiology Axonal Branching Actin Trail FMN2 Actin Patch |
Issue Date: | Jun-2019 |
Abstract: | Axonal branching process is an essential mechanism for forming complex neural circuits by facilitating in the formation of multiple synaptic connections with multiple target-fields. Even though the axonal branching mechanism is still poorly understood, several potential candidates might have a role in the axonal branching process, but our attention went to FMN2 protein due to its increased expression level in the nervous system of mammals and few studies implicating FMN2 with intellectual disabilities. FMN2 is actin nucleation and elongation protein from a well-known Protein family called Formins. There are studies confirming FMN2 being an actin bundling and microtubule interacting protein. These diverse functions with the cytoskeletal system found to be useful in an axonal branching process. From this project, actin nucleation and elongation activity of FMN2 was found to be regulating the protrusive activity. The actin patch majorly governs initiation of a protrusion and FMN2 was found to be influencing actin patch dynamics also. Depletion of FMN2 in neurons significantly reduced the lifetime and area of actin patch in the axon shaft and by overexpressing the FMN2 in neurons displayed a distinguishable increase in actin patch lifetime. Still, there is a lot to be understood about axonal branching mechanism from the perspective of FMN2. Hence this project is going ahead in search of that. |
URI: | http://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/3095 |
Appears in Collections: | MS THESES |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
5th Year MS Thesis Sooraj S Das(20141080).pdf | 3.11 MB | Adobe PDF | View/Open |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.