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Fertilization is a key event for sexually reproducing plants. Pollen–stigma adhesion, which is the first step in male–female interaction during fertilization, requires proper pollen wall patterning. Callose, which is a β-1.3-glucan, is an essential polysaccharide that is required for pollen development and pollen wall formation. Mutations in <i>CALLOSE SYNTHASE 5</i> (<i>CalS5</i>) disrupt male meiotic callose accumulation; however, how CalS5 activity and callose synthesis are regulated is not fully understood. In this paper, we report the isolation of a <i>kompeito-1</i> (<i>kom-1</i>) mutant defective in pollen wall patterning and pollen–stigma adhesion in <i>Arabidopsis thaliana</i>. Callose was not accumulated in <i>kom-1</i> meiocytes or microspores, which was very similar to the <i>cals5</i> mutant. The <i>KOM</i> gene encoded a member of a subclass of Rhomboid serine protease proteins that lacked active site residues. KOM was localized to the Golgi apparatus, and both <i>KOM</i> and <i>CalS5</i> genes were highly expressed in meiocytes. A 220 kDa CalS5 protein was detected in wild-type (Col-0) floral buds but was dramatically reduced in <i>kom-1</i>. These results suggested that KOM was required for CalS5 protein accumulation, leading to the regulation of meiocyte-specific callose accumulation and pollen wall formation.