TY - GEN A1 - Huu, Cuong Nguyen A1 - Plaschil, Sylvia A1 - Himmelbach, Axel A1 - Kappel, Christian A1 - Lenhard, Michael T1 - Female self-incompatibility type in heterostylous Primula is determined by the brassinosteroid-inactivating cytochrome P450 CYP734A50 T2 - Current biology N2 - Most flowering plants are hermaphrodites, with flowers having both male and female reproductive organs. One widespread adaptation to limit self-fertilization is self-incompatibility (SI), where self-pollen fails to fertilize ovules.(1,2) In homomorphic SI, many morphologically indistinguishable mating types are found, although in heteromorphic SI, the two or three mating types are associated with different floral morphologies.(3-6) In heterostylous Primula, a hemizygous supergene determines a short-styled S-morph and a long-styled L-morph, corresponding to two different mating types, and full seed set only results from inter morph crosses.(7-9) Style length is controlled by the brassinosteroid (BR)-inactivating cytochrome P450 CYP734A50,(10) yet it remains unclear what defines the male and female incompatibility types. Here, we show that CYP734A50 also determines the female incompatibility type. Inactivating CYP734A50 converts short S-morph styles into long styles with the same incompatibility behavior as L-morph styles, and this effect can be mimicked by exogenous BR treatment. In vitro responses of S-and L-morph pollen grains and pollen tubes to increasing BR levels could only partly explain their different in vivo behavior, suggesting both direct and indirect effects of the different BR levels in S-versus L-morph stigmas and styles in controlling pollen performance. This BR-mediated SI provides a novel mechanism for preventing self-fertilization. The joint control of morphology and SI by CYP734A50 has important implications for the evolutionary buildup of the heterostylous syndrome and provides a straightforward explanation for why essentially all of the derived self-compatible homostylous Primula species are long homostyles.(11) KW - heteromorphic self-incompatibility KW - heterostyly KW - Primula forbesii KW - brassinosteroid KW - CYP734A50 KW - supergene KW - pleiotropy Y1 - 2022 U6 - https://doi.org/10.1016/j.cub.2021.11.046 SN - 0960-9822 SN - 1879-0445 VL - 32 IS - 3 SP - 671 EP - 676, E1-E5 PB - Cell Press CY - Cambridge, Mass. ER - TY - JOUR A1 - Jöst, Moritz A1 - Hensel, Goetz A1 - Kappel, Christian A1 - Druka, Arnis A1 - Sicard, Adrien A1 - Hohmann, Uwe A1 - Beier, Sebastian A1 - Himmelbach, Axel A1 - Waugh, Robbie A1 - Kumlehn, Jochen A1 - Stein, Nils A1 - Lenhard, Michael T1 - The INDETERMINATE DOMAIN Protein BROAD LEAF1 Limits Barley Leaf Width by Restricting Lateral Proliferation JF - Current biology N2 - Variation in the size, shape, and positioning of leaves as the major photosynthetic organs strongly impacts crop yield, and optimizing these aspects is a central aim of cereal breeding [1, 2]. Leaf growth in grasses is driven by cell proliferation and cell expansion in a basal growth zone [3]. Although several factors influencing final leaf size and shape have been identified from rice and maize [4-14], what limits grass leaf growth in the longitudinal or transverse directions during leaf development remains poorly understood. To identify factors involved in this process, we characterized the barley mutant broad leaf1 (blf1). Mutants form wider but slightly shorter leaves due to changes in the numbers of longitudinal cell files and of cells along the leaf length. These differences arise during primordia outgrowth because of more cell divisions in the width direction increasing the number of cell files. Positional cloning, analysis of independent alleles, and transgenic complementation confirm that BLF1 encodes a presumed transcriptional regulator of the INDETERMINATE DOMAIN family. In contrast to loss-of-function mutants, moderate overexpression of BLF1 decreases leaf width below wild-type levels. A functional BLF1-vYFP fusion protein expressed from the endogenous promoter shows a dynamic expression pattern in the shoot apical meristem and young leaf primordia. Thus, we propose that the BLF1 gene regulates barley leaf size by restricting cell proliferation in the leaf-width direction. Given the agronomic importance of canopy traits in cereals, identifying functionally different BLF1 alleles promises to allow for the generation of optimized cereal ideotypes. Y1 - 2016 U6 - https://doi.org/10.1016/j.cub.2016.01.047 SN - 0960-9822 SN - 1879-0445 VL - 26 SP - 903 EP - 909 PB - Cell Press CY - Cambridge ER - TY - JOUR A1 - Cuong Nguyen Huu, A1 - Kappel, Christian A1 - Keller, Barbara A1 - Sicard, Adrien A1 - Takebayashi, Yumiko A1 - Breuninger, Holger A1 - Nowak, Michael D. A1 - Bäurle, Isabel A1 - Himmelbach, Axel A1 - Burkart, Michael A1 - Ebbing-Lohaus, Thomas A1 - Sakakibara, Hitoshi A1 - Altschmied, Lothar A1 - Conti, Elena A1 - Lenhard, Michael T1 - Presence versus absence of CYP734A50 underlies the style-length dimorphism in primroses JF - eLife N2 - Heterostyly is a wide-spread floral adaptation to promote outbreeding, yet its genetic basis and evolutionary origin remain poorly understood. In Primula (primroses), heterostyly is controlled by the S-locus supergene that determines the reciprocal arrangement of reproductive organs and incompatibility between the two morphs. However, the identities of the component genes remain unknown. Here, we identify the Primula CYP734A50 gene, encoding a putative brassinosteroid-degrading enzyme, as the G locus that determines the style-length dimorphism. CYP734A50 is only present on the short-styled S-morph haplotype, it is specifically expressed in S-morph styles, and its loss or inactivation leads to long styles. The gene arose by a duplication specific to the Primulaceae lineage and shows an accelerated rate of molecular evolution. Thus, our results provide a mechanistic explanation for the Primula style-length dimorphism and begin to shed light on the evolution of the S-locus as a prime model for a complex plant supergene. Y1 - 2016 U6 - https://doi.org/10.7554/eLife.17956 SN - 2050-084X VL - 5 PB - eLife Sciences Publications CY - Cambridge ER -