Control of plant germline proliferation by SCFFBL17 degradation of cell cycle inhibitors

Flowering plants: doubly fertile Double fertilization is a biologically unique reproduction system considered a key innovation in the evolution of flowering plants. Unlike fertilization in animals, double fertilization involves the production of a pair of sperm cells by the selective division of unequal daughter cells. Now a novel F-box protein, FBL17, has been found to promote twin sperm cell production in Arabidopsis. FBL17 targets KRP7, an inhibitor of cyclin-dependent kinases, in the male germ cells. The cell cycle regulation mechanism used by flowering plants is evolutionarily conserved between yeast and animal cells, and this new work shows how regulatory mechanisms have evolved to tailor it to special circumstances. A newly discovered F-box protein of Arabidopsis thaliana that promotes twin sperm cell production is identified. The protein, FBL17, targets KRP7, an Arabidopsis inhibitor of CDKA1, for proteasome-dependent degradation, allowing germ cell division and twin sperm cell production. Flowering plants possess a unique reproductive strategy, involving double fertilization by twin sperm cells 1 . Unlike animal germ lines, the male germ cell lineage in plants only forms after meiosis and involves asymmetric division of haploid microspores, to produce a large, non-germline vegetative cell and a germ cell that undergoes one further division to produce the twin sperm cells 2 . Although this switch in cell cycle control is critical for sperm cell production and delivery, the underlying molecular mechanisms are unknown. Here we identify a novel F-box protein of Arabidopsis thaliana , designated FBL17 (F-box-like 17), that enables this switch by targeting the degradation of cyclin-dependent kinase A;1 inhibitors specifically in male germ cells. We show that FBL17 is transiently expressed in the male germ line after asymmetric division and forms an SKP1–Cullin1–F-box protein (SCF) E3 ubiquitin ligase complex (SCF FBL17 ) that targets the cyclin-dependent kinase inhibitors KRP6 and KRP7 for proteasome-dependent degradation. Accordingly, the loss of FBL17 function leads to the stabilization of KRP6 and inhibition of germ cell cycle progression. Our results identify SCF FBL17 as an essential male germ cell proliferation complex that promotes twin sperm cell production and double fertilization in flowering plants.