Diversity and selection of the continuous-flowering gene, RoKSN, in rose.

Blooming seasonality is an important trait in ornamental plants and was selected by humans. Wild roses flower only in spring whereas most cultivated modern roses can flower continuously. This trait is explained by a mutation of a floral repressor gene, RoKSN, a TFL1 homologue. In this work, we studied the origin, the diversity and the selection of the RoKSN gene. We analyzed 270 accessions, including wild and old cultivated Asian and European roses as well as modern roses. By sequencing the RoKSN gene, we proposed that the allele responsible for continuous-flowering, RoKSNcopia, originated from Chinese wild roses (Indicae section), with a recent insertion of the copia element. Old cultivated Asian roses with the RoKSNcopia allele were introduced in Europe, and the RoKSNcopia allele was progressively selected during the 19th and 20th centuries, leading to continuous-flowering modern roses. Furthermore, we detected a new allele, RoKSNA181, leading to a weak reblooming. This allele encodes a functional floral repressor and is responsible for a moderate accumulation of RoKSN transcripts. A transient selection of this RoKSNA181 allele was observed during the 19th century. Our work highlights the selection of different alleles at the RoKSN locus for recurrent blooming in rose.

OSD1 promotes meiotic progression via APC/C inhibition and forms a regulatory network with TDM and CYCA1;2/TAM.

Cell cycle control is modified at meiosis compared to mitosis, because two divisions follow a single DNA replication event. Cyclin-dependent kinases (CDKs) promote progression through both meiosis and mitosis, and a central regulator of their activity is the APC/C (Anaphase Promoting Complex/Cyclosome) that is especially required for exit from mitosis. We have shown previously that OSD1 is involved in entry into both meiosis I and meiosis II in Arabidopsis thaliana; however, the molecular mechanism by which OSD1 controls these transitions has remained unclear. Here we show that OSD1 promotes meiotic progression through APC/C inhibition. Next, we explored the functional relationships between OSD1 and the genes known to control meiotic cell cycle transitions in Arabidopsis. Like osd1, cyca1;2/tam mutation leads to a premature exit from meiosis after the first division, while tdm mutants perform an aberrant third meiotic division after normal meiosis I and II. Remarkably, while tdm is epistatic to tam, osd1 is epistatic to tdm. We further show that the expression of a non-destructible CYCA1;2/TAM provokes, like tdm, the entry into a third meiotic division. Finally, we show that CYCA1;2/TAM forms an active complex with CDKA;1 that can phosphorylate OSD1 in vitro. We thus propose that a functional network composed of OSD1, CYCA1;2/TAM, and TDM controls three key steps of meiotic progression, in which OSD1 is a meiotic APC/C inhibitor.