TY  - JOUR
A1  - Brzezinka, Krzysztof
A1  - Altmann, Simone
A1  - Czesnick, Hjördis
A1  - Nicolas, Philippe
A1  - Gorka, Michal
A1  - Benke, Eileen
A1  - Kabelitz, Tina
A1  - Jähne, Felix
A1  - Graf, Alexander
A1  - Kappel, Christian
A1  - Bäurle, Isabel
T1  - Arabidopsis FORGETTER1 mediates stress-induced chromatin memory through nucleosome remodeling
JF  - eLife
N2  - Plants as sessile organisms can adapt to environmental stress to mitigate its adverse effects. As part of such adaptation they maintain an active memory of heat stress for several days that promotes a more efficient response to recurring stress. We show that this heat stress memory requires the activity of the FORGETTER1 (FGT1) locus, with fgt1 mutants displaying reduced maintenance of heat-induced gene expression. FGT1 encodes the Arabidopsis thaliana orthologue of Strawberry notch (Sno), and the protein globally associates with the promoter regions of actively expressed genes in a heat-dependent fashion. FGT1 interacts with chromatin remodelers of the SWI/ SNF and ISWI families, which also display reduced heat stress memory. Genomic targets of the BRM remodeler overlap significantly with FGT1 targets. Accordingly, nucleosome dynamics at loci with altered maintenance of heat-induced expression are affected in fgt1. Together, our results suggest that by modulating nucleosome occupancy, FGT1 mediates stress-induced chromatin memory.
Y1  - 2016
U6  - https://doi.org/10.7554/eLife.17061
SN  - 2050-084X
VL  - 5
PB  - eLife Sciences Publications
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  - 
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  - Kabelitz, Tina
A1  - Brzezinka, Krzysztof
A1  - Friedrich, Thomas
A1  - Gorka, Michal
A1  - Graf, Alexander
A1  - Kappel, Christian
A1  - Bäurle, Isabel
T1  - A JUMONJI Protein with E3 Ligase and Histone H3 Binding Activities Affects Transposon Silencing in Arabidopsis
JF  - Plant physiology : an international journal devoted to physiology, biochemistry, cellular and molecular biology, biophysics and environmental biology of plants
N2  - Transposable elements (TEs) make up a large proportion of eukaryotic genomes. As their mobilization creates genetic variation that threatens genome integrity, TEs are epigenetically silenced through several pathways, and this may spread to neighboring sequences. JUMONJI (JMJ) proteins can function as antisilencing factors and prevent silencing of genes next to TEs. Whether TE silencing is counterbalanced by the activity of antisilencing factors is still unclear. Here, we characterize JMJ24 as a regulator of TE silencing. We show that loss of JMJ24 results in increased silencing of the DNA transposon AtMu1c, while overexpression of JMJ24 reduces silencing. JMJ24 has a JumonjiC (JmjC) domain and two RING domains. JMJ24 autoubiquitinates in vitro, demonstrating E3 ligase activity of the RING domain(s). JMJ24-JmjC binds the N-terminal tail of histone H3, and full-length JMJ24 binds histone H3 in vivo. JMJ24 activity is anticorrelated with histone H3 Lys 9 dimethylation (H3K9me2) levels at AtMu1c. Double mutant analyses with epigenetic silencing mutants suggest that JMJ24 antagonizes histone H3K9me2 and requires H3K9 methyltransferases for its activity on AtMu1c. Genome-wide transcriptome analysis indicates that JMJ24 affects silencing at additional TEs. Our results suggest that the JmjC domain of JMJ24 has lost demethylase activity but has been retained as a binding domain for histone H3. This is in line with phylogenetic analyses indicating that JMJ24 (with the mutated JmjC domain) is widely conserved in angiosperms. Taken together, this study assigns a role in TE silencing to a conserved JmjC-domain protein with E3 ligase activity, but no demethylase activity.
Y1  - 2016
U6  - https://doi.org/10.1104/pp.15.01688
SN  - 0032-0889
SN  - 1532-2548
VL  - 171
SP  - 344
EP  - 358
PB  - American Society of Plant Physiologists
CY  - Rockville
ER  - 
TY  - JOUR
A1  - Sas, Claudia
A1  - Mueller, Frank
A1  - Kappel, Christian
A1  - Kent, Tyler V.
A1  - Wright, Stephen I.
A1  - Hilker, Monika
A1  - Lenhard, Michael
T1  - Repeated Inactivation of the First Committed Enzyme Underlies the Loss of Benzaldehyde Emission after the Selfing Transition in Capsella
JF  - Current biology
N2  - The enormous species richness of flowering plants is at least partly due to floral diversification driven by interactions between plants and their animal pollinators [1, 2]. Specific pollinator attraction relies on visual and olfactory floral cues [3-5]; floral scent can not only attract pollinators but also attract or repel herbivorous insects [6-8]. However, despite its central role for plant-animal interactions, the genetic control of floral scent production and its evolutionary modification remain incompletely understood [9-13]. Benzenoids are an important class of floral scent compounds that are generated from phenylalanine via several enzymatic pathways [14-17]. Here we address the genetic basis of the loss of floral scent associated with the transition from outbreeding to selfing in the genus Capsella. While the outbreeding C. grandiflora emits benzaldehyde as a major constituent of its floral scent, this has been lost in the selfing C. rubella. We identify the Capsella CNL1 gene encoding cinnamate: CoA ligase as responsible for this variation. Population genetic analysis indicates that CNL1 has been inactivated twice independently in C. rubella via different novel mutations to its coding sequence. Together with a recent study in Petunia [18], this identifies cinnamate: CoA ligase as an evolutionary hotspot for mutations causing the loss of benzenoid scent compounds in association with a shift in the reproductive strategy of Capsella from pollination by insects to self-fertilization.
Y1  - 2016
U6  - https://doi.org/10.1016/j.cub.2016.10.026
SN  - 0960-9822
SN  - 1879-0445
VL  - 26
SP  - 3313
EP  - 3319
PB  - Cell Press
CY  - Cambridge
ER  - 
TY  - JOUR
A1  - Sicard, Adrien
A1  - Kappel, Christian
A1  - Lee, Young Wha
A1  - Wozniak, Natalia Joanna
A1  - Marona, Cindy
A1  - Stinchcombe, John R.
A1  - Wright, Stephen I.
A1  - Lenhard, Michael
T1  - Standing genetic variation in a tissue-specific enhancer underlies
selfing-syndrome evolution in Capsella
JF  - Proceedings of the National Academy of Sciences of the United States of America
N2  - Mating system shifts recurrently drive specific changes in organ dimensions. The shift in mating system from out-breeding to selfing is one of the most frequent evolutionary transitions in flowering plants and is often associated with an organ-specific reduction in flower size. However, the evolutionary paths along which polygenic traits, such as size, evolve are poorly understood. In particular, it is unclear how natural selection can specifically modulate the size of one organ despite the pleiotropic action of most known growth regulators. Here, we demonstrate that allelic variation in the intron of a general growth regulator contributed to the specific reduction of petal size after the transition to selfing in the genus Capsella. Variation within this intron affects an organ-specific enhancer that regulates the level of STERILE APETALA (SAP) protein in the developing petals. The resulting decrease in SAP activity leads to a shortening of the cell proliferation period and reduced number of petal cells. The absence of private polymorphisms at the causal region in the selfing species suggests that the small-petal allele was captured from standing genetic variation in the ancestral out-crossing population. Petal-size variation in the current out-crossing population indicates that several small-effect mutations have contributed to reduce petal-size. These data demonstrate how tissue-specific regulatory elements in pleiotropic genes contribute to organ-specific evolution. In addition, they provide a plausible evolutionary explanation for the rapid evolution of flower size after the out-breeding-to-selfing transition based on additive effects of segregating alleles.
KW  - morphological evolution
KW  - growth control
KW  - standing variation;
 organ-specific evolution
KW  - intronic cis-regulatory element
Y1  - 2016
U6  - https://doi.org/10.1073/pnas.1613394113
SN  - 0027-8424
VL  - 113
SP  - 13911
EP  - 13916
PB  - National Acad. of Sciences
CY  - Washington
ER  -