Abstract
Sterols are essential lipids for plant growth, and the sterol content is tightly regulated by a fail-safe system consisting of two processes: 1) suppression of excess sterol production by a negative regulator of sterol biosynthesis (HIGR STEROL ESTER 1, HISE1), and 2) conversion of excess sterols to sterol esters by PHOSPHOLIPID STEROL ACYLTRANSFERASE 1 (PSAT1) in Arabidopsis thaliana. The hise1-3 psat1-2 double mutant has a 1.5-fold higher sterol content in leaves than the wild type; this upregulates the expression of stress-responsive genes, leading to disruption of cellular activities in leaves. However, the effects of excess sterols on seeds are largely unknown. Here, we show that excess sterols cause multiple defects in seeds. The seeds of hise1-3 psat1-2 plants had a higher sterol content than wild-type seeds and showed a deeper color than wild-type seeds because of the accumulation of proanthocyanidin. The seed coat in the hise1-3 psat1-2 mutant was abnormally wrinkled. Seed coat formation is accompanied by cell death-mediated shrinkage of the inner integument. In the hise1-3 psat1-2 mutant, transmission electron microscopy showed that shrinkage of the integument was impaired, resulting in a thick seed coat and delayed seed germination. Moreover, psat1-2 and hise1-3 psat1-2 seeds displayed defective imbibition. Taken together, the results suggest that excess sterols impair proper seed coat formation, thereby inhibiting seed germination.