Germband extension during Drosophila development is primarily driven by cell intercalation, which involves three key components: planar cell polarity, anisotropic myosin contractile forces on cellular junctions, and cellular deformation and movement. Prior experimental work probed each of these factors in depth, but the connection between them remains unclear. This paper presents an integrated chemomechanical model that combines the three factors into a coherent mathematical framework for studying cell intercalation in the germband tissue. The model produces the planar cell polarization of key proteins, including Rho-kinase, Bazooka and myosin, the development of anisotropic contractile forces, and subsequent cell deformation and rearrangement. Cell intercalation occurs through T1 transitions among four neighboring cells and rosettes involving six cells. Such six-cell rosettes entail stronger myosin-based contractile forces, and on average produce a moderately larger amount of germband extension than the T1 transitions. The resolution of T1 and rosettes is driven by contractile forces on junctions anterior and posterior to the assembly as well as the pulling force of the medial myosin in the anterior and posterior cells. The global stretching due to posterior midgut invagination also plays a minor role. These model predictions are in reasonable agreement with experimental observations.