Disruption and overexpression of Arabidopsis phytosulfokine receptor gene affects cellular longevity and potential for growth.

Phytosulfokine (PSK), a 5-amino acid sulfated peptide that has been identified in conditioned medium of plant cell cultures, promotes cellular growth in vitro via binding to the membrane-localized PSK receptor. Here, we report that loss-of-function and gain-of-function mutations of the Arabidopsis (Arabidopsis thaliana) PSK receptor gene (AtPSKR1) alter cellular longevity and potential for growth without interfering with basic morphogenesis of plants. Although mutant pskr1-1 plants exhibit morphologically normal growth until 3 weeks after germination, individual pskr1-1 cells gradually lose their potential to form calluses as tissues mature. Shortly after a pskr1-1 callus forms, it loses potential for growth, resulting in formation of a smaller callus than the wild type. Leaves of pskr1-1 plants exhibit premature senescence after bolting. Leaves of AtPSKR1ox plants exhibit greater longevity and significantly greater potential for callus formation than leaves of wild-type plants, irrespective of their age. Calluses derived from AtPSKR1ox plants maintain their potential for growth longer than wild-type calluses. Combined with our finding that PSK precursor genes are more strongly expressed in mature plant parts than in immature plant parts, the available evidence indicates that PSK signaling affects cellular longevity and potential for growth and thereby exerts a pleiotropic effect on cultured tissue in response to environmental hormonal conditions.

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