After spinal cord injury (SCI), astrocytes become reactive in a process called astrogliosis. These reactive astrocytes surround the lesion and form an astrocyte scar border. Our lab recently previously discovered that LZK (or MAP3K13) regulates reactive astrogliosis and scar formation after a dorsal spinal cord crush injury. The effect of LZK-mediated astrogliosis on neural repair and regeneration is still not clear. We aim to investigate this question utilizing genetically modified mice and RNA sequencing. We are testing the effect of astrocytic LZK overexpression or deletion on behavioral recovery after a contusion injury. We will also assess the effect of the same LZK manipulations on corticospinal tract (CST) axon regeneration that is induced by Pten suppression or IGF1/OPN overexpression. To identify potential downstream effectors of LZK signaling, we are setting up the RiboTag approach to examine the transcriptomic profiles of LZK-manipulated astrocytes. The relationship between the LZK and STAT3 pathways are also being examined with genetic analyses. Studying LZK-mediated astrogliosis provides an opportunity to dive deep into the mechanisms involved in astrocyte border formation and function. Together, these experiments will provide important insight into the cellular and molecular processes involved in astrogliosis and its functional consequences in SCI, which provides the basis for developing effective therapeutic interventions for spinal cord injury in the future.