Small RNA molecules called microRNAs (miRNAs) are translational repressors and are involved in a variety of processes important for normal cell development and function. Previous studies in our lab showed that miRNAs are required in early (embryonic) stages of retinal development. After depletion of miRNAs in early retinal progenitor cells (RPCs), late RPCs and their progeny, such as Müller glia (MG) which are the primary glial in the retina, are not generated. Instead, only early born neurons are produced. The depletion of miRNAs can be obtained through deletion of an enzyme that generates mature miRNAs called Dicer. Since we know that miRNAs are crucial for early retinal development, this study investigated if miRNAs are also important for proper late (postnatal) retinal development. We used a Sox2 reporter mouse which allows visualizing late retinal progenitors (Sox2 is a gene expressed in RPCs) and selectively deleted Dicer in RPCs at postnatal day 2-6. The tissue was analyzed 2, 4 and 7.5 weeks after Dicer deletion and compared to normal retinas using immunofluorescent staining of retinal cross sections and confocal microscopy. We found massive disruptions in the retinal architecture such as the formation of rosette/ bubble-like structures, indicating that miRNAs are required for proper formation of the retinal layers. Since MG play a role in maintaining the retinal structure, in a second series of experiments we induced Dicer deletion specifically in MG at postnatal day 11 –14, when the retina is almost completely developed. The tissue was analyzed 8 and 20 weeks after Dicer-deletion and compared to normal tissue. We found an atypical location of MG and disruptions in the layered retinal structure, indicating that miRNAs are also required for accurate MG location in the retina, which is essential for normal retinal architecture.