The suprachiasmatic nucleus (SCN) of the anterior hypothalamus is the main clock that governs circadian (~24 h) behaviors in mammals. Although each neuron in the SCN is capable of circadian timekeeping, it is the property of the whole SCN tissue that enables coding of time beyond the circadian domain, such as the seasons. What is the origin of plasticity required for this coding? We suggest that, unlike the cortical microcircuits, the plasticity in the hypothalamic network may not be in the synapse but lie in the soma. We monitored spatial gene expression oscillations in the cultured SCN from mice entrained to seasonal daylength conditions mimicking winter (8:16 h light:dark), summer (12:8), and the equinox (12:12). We observed that the SCN is composed of two clusters of fast and slow paced clocks with a distinct spatial distribution, which was not altered by the daylength. However, the phase gap between the clusters became the largest in the summer daylength entrained group and the shortest in the winter group. When a cluster is cultured in isolation, the fast paced cluster under the equinox condition became even faster under summer and slower under winter daylength condition. We propose a simple model that demonstrates how these seasonal changes in the cluster period accounts for phase reorganization. The modulation of circadian period that occurs in the soma appears the major contributor to seasonal timing. We find this interpretation consistent with a longstanding hypothesis that the 'clock for all seasons' comes from the organization of periods and phases of two independent oscillators (Daan and Pittendrigh, 1976).