Over half of the interneurons in the mouse olfactory bulb (OB) are developed during the first week after birth, and dominantly connect to excitatory tufted cells near the superficial granule cell layer (sGCL), unlike late-born interneurons. However, the molecular mechanisms underlying the temporal specification have not been identified. Here, we discover the role of Abelson Tyrosine-Protein Kinase 1 (Abl1) in the temporal development of early-born OB interneurons. Lentiviral knockdown of Abl1 disrupts sGCL-specific circuit of the early-born interneurons by integratory and functional defects, resulting in olfactory hyper-sensitivity. From a proteomics approach, we find that Doublecortin (Dcx) is phosphorylated by Abl1, and which contributes to the stabilization of Dcx, thereby regulating microtubule dynamics. Finally, Dcx overexpression rescues Abl1-knockdown-induced anatomic or functional defects. In summary, we suggest that the specific signaling of Abl1-Dcx in early-born interneurons facilitates the temporal development of sGCL circuit for regulating innate olfactory functions, such as detection and sensitivity.