Abstract
Key message
The split-hull phenotype caused by reduced lemma width and low lignin content is under control of
SPH
encoding a type-2 13-lipoxygenase and contributes to high dehulling efficiency.
Rice hulls consist of two bract-like structures, the lemma and palea. The hull is an important organ that helps to protect seeds from environmental stress, determines seed shape, and ensures grain filling. Achieving optimal hull size and morphology is beneficial for seed development. We characterized the
split
-
hull
(
sph
) mutant in rice, which exhibits hull splitting in the interlocking part between lemma and palea and/or the folded part of the lemma during the grain filling stage. Morphological and chemical analysis revealed that reduction in the width of the lemma and lignin content of the hull in the
sph
mutant might be the cause of hull splitting. Genetic analysis indicated that the mutant phenotype was controlled by a single recessive gene,
sph
(
Os04g0447100
), which encodes a type-2 13-lipoxygenase.
SPH
knockout and knockdown transgenic plants displayed the same split-hull phenotype as in the mutant. The
sph
mutant showed significantly higher linoleic and linolenic acid (substrates of lipoxygenase) contents in spikelets compared to the wild type. It is probably due to the genetic defect of
SPH
and subsequent decrease in lipoxygenase activity. In dehulling experiment, the
sph
mutant showed high dehulling efficiency even by a weak tearing force in a dehulling machine. Collectively, the results provide a basis for understanding of the functional role of lipoxygenase in structure and maintenance of hulls, and would facilitate breeding of easy-dehulling rice.