Astrocytes are glial cells with critical roles in brain development, maturation, homeostasis, and plasticity, and dysregulations in astrocytes contribute to neurodevelopmental and neurologic disorders. This dissertation investigates the role of astrocytes in the neurodevelopmental disorder fragile X syndrome (FXS) as well as in the heterogeneity and development of the cortex. I used mouse genetic tools to suppress astrocyte bone morphogenetic protein (BMP) signaling in vivo, and ask how this suppression affected fragile x syndrome molecular, functional, and behavioral phenotypes as well as cortical astrocyte heterogeneity and development. Chapter 2 describes generation and validation of the model to suppress astrocyte BMP signaling with astrocyte-specific conditional knock out (cKO) of Smad4, and identifies transcriptomic changes in both typical and FXS-affected cortical astrocytes with or without BMP signaling. I find that FXS-affected astrocytes have an overall hypermetabolic transcriptomic signature that is moderated by Smad4 cKO. Chapter 3 describes development of a method to profile astrocyte secreted and membrane proteins in vivo, and identifies proteomic changes in both typical and FXS-affected cortical astrocytes with or without BMP signaling. I find that FXS-affected astrocytes have downregulated secretory machinery and secreted proteins, with these alterations reversed by Smad4 cKO. Chapter 4 asks whether Smad4 cKO can rescue FXS functional phenotypes. I find that Smad4 cKO lessens severity of audiogenic seizures in FXS mice, does not affect FXS visual acuity or ocular dominance plasticity, and restores deficits in inhibitory synapses present in FXS auditory cortex. Chapter 5 investigates the role of astrocyte BMP signaling in healthy development, applying transcriptomic and proteomic data from previous chapters. I find that Smad4-dependent BMP signaling is necessary for spatially-segregated astrocyte transcriptomic variability and in particular pial astrocyte gene signatures, and that BMP signaling mediates aspects of astrocyte and cortical maturation. These data demonstrate that astrocytes contribute to FXS molecular and functional phenotypes, that targeting astrocyte BMP signaling can mitigate FXS symptoms, and that astrocyte BMP signaling affects cortical heterogeneity and development. Overall, this dissertation demonstrates that an astrocyte signaling pathway mediates both aspects of healthy development as well as molecular and functional changes in a genetic disorder.