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Abstract Master transcription factors reprogram cell fate in multicellular eukaryotes. Pioneer transcription factors have prominent roles in this process because of their ability to contact their cognate binding motifs in closed chromatin. Reprogramming is pervasive in plants, whose development is plastic and tuned by the environment, yet little is known about pioneer transcription factors in this kingdom. Here, we show that the master transcription factor LEAFY (LFY), which promotes floral fate through upregulation of the floral commitment factor APETALA1 ( AP1 ), is a pioneer transcription factor. In vitro, LFY binds to the endogenous AP1 target locus DNA assembled into a nucleosome. In vivo, LFY associates with nucleosome occupied binding sites at the majority of its target loci, including AP1 . Upon binding, LFY ‘unlocks’ chromatin locally by displacing the H1 linker histone and by recruiting SWI/SNF chromatin remodelers, but broad changes in chromatin accessibility occur later. Our study provides a mechanistic framework for patterning of inflorescence architecture and uncovers striking similarities between LFY and animal pioneer transcription factor. 

Abstract This year marks the 100 th anniversary of the experiments by Garner and Allard (Garner and Allard, 1920) that showed that plants measure the duration of the night and day (the photoperiod) to time flowering. This discovery led to the identification of Flowering Locus T (FT) in Arabidopsis and Heading Date 3a (Hd3a) in rice as a mobile signal that promotes flowering in tissues distal to the site of cue perception. FT/Hd3a belong to the family of phosphatidylethanolamine binding proteins (PEBPs). Collectively, these proteins control plant developmental transitions and plant architecture. Several excellent recent reviews have focused on the roles of PEBP proteins in diverse plant species; here we will primarily highlight recent advances that enhance our understanding of the mechanism of action of PEBP proteins and discuss critical open questions. 

Plants monitor seasonal cues to optimize reproductive success by tuning onset of reproduction and inflorescence architecture. TERMINAL FLOWER 1 (TFL1) and FLOWERING LOCUS T (FT) and their orthologs antagonistically regulate these life history traits, yet their mechanism of action, antagonism and targets remain poorly understood. Here, we show that TFL1 is recruited to thousands of loci by the bZIP transcription factor FD. We identify the master regulator of floral fate,LEAFY(LFY) as a target under dual opposite regulation by TFL1 and FT and uncover a pivotal role of FT in promoting flower fate viaLFYupregulation. We provide evidence that the antagonism between FT and TFL1 relies on competition for chromatin-bound FD at shared target loci. Direct TFL1-FD regulated target genes identify this complex as a hub for repressing both master regulators of reproductive development and endogenous signalling pathways. Our data provide mechanistic insight into how TFL1-FD sculpt inflorescence architecture, a trait important for reproductive success, plant architecture and yield.

 

Abstract The promise of high-density and low-energy-consumption devices motivates the search for layered structures that stabilize chiral spin textures such as topologically protected skyrmions. At the same time, recently discovered long-range intrinsic magnetic orders in the two-dimensional van der Waals materials provide a new platform for the discovery of novel physics and effects. Here we demonstrate the Dzyaloshinskii–Moriya interaction and Néel-type skyrmions are induced at the WTe 2 /Fe 3 GeTe 2 interface. Transport measurements show the topological Hall effect in this heterostructure for temperatures below 100 K. Furthermore, Lorentz transmission electron microscopy is used to directly image Néel-type skyrmion lattice and the stripe-like magnetic domain structures as well. The interfacial coupling induced Dzyaloshinskii–Moriya interaction is estimated to have a large energy of 1.0 mJ m −2 . This work paves a path towards the skyrmionic devices based on van der Waals layered heterostructures. 

Abstract Specification of new organs from transit amplifying cells is critical for higher eukaryote development. In plants, a central stem cell pool maintained by the pluripotency factor SHOOTMERISTEMLESS (STM), is surrounded by transit amplifying cells competent to respond to auxin hormone maxima by giving rise to new organs. Auxin triggers flower initiation through Auxin Response Factor (ARF) MONOPTEROS (MP) and recruitment of chromatin remodelers to activate genes promoting floral fate. The contribution of gene repression to reproductive primordium initiation is poorly understood. Here we show that downregulation of the STM pluripotency gene promotes initiation of flowers and uncover the mechanism for STM silencing. The ARFs ETTIN (ETT) and ARF4 promote organogenesis at the reproductive shoot apex in parallel with MP via histone-deacetylation mediated transcriptional silencing of STM . ETT and ARF4 directly repress STM , while MP acts indirectly, through its target FILAMENTOUS FLOWER ( FIL ). Our data suggest that – as in animals- downregulation of the pluripotency program is important for organogenesis in plants. 

For degradable magnesium (Mg) alloy‐based stents it would be desirable to delay early corrosion to maintain mechanical strength. Similarly, early after stent placement reduced thrombogenicity is an important feature, while chronically, endothelial cell adhesion and vessel integration are desirable. In this study, surface eroding polymers of amino‐grafted poly(1,3‐trimethylene carbonate) (PTMC‐NH₂) and PTMC‐NH₂combined with sulfobetaine bearing polymer PSB (PTMC‐NHCO‐PSB) are developed, and these polymers are covalently attached onto 6‐phosphonohexanoic acid (PHA)‐coated AZ31 Mg alloy surfaces in sequence. In vitro degradation testing in ovine plasma shows PTMC, PTMC‐NH₂, and PTMC‐NHCO‐PSB cast films experience a gradual thickness and mass loss with maintenance of smooth surfaces, confirming surface erosion behavior. The PTMC‐NH₂polymer is firmly bound to the PHA‐modified AZ31 surface and demonstrates a resistance to peeling. PTMC, PTMC‐NH₂, and PTMC‐NHCO‐PSB coated AZ31 have a lower corrosion rate versus polylactide‐co‐glycolide coated and untreated AZ31. PTMC‐NHCO‐PSB coated AZ31 inhibits platelet deposition and smooth muscle cell adhesion and growth, but after 2‐week immersion in plasma, this surface supports endothelial cell adhesion and growth. These results suggest PTMC‐NHCO‐PSB surface eroding coating offers a means of controlling corrosion while providing a temporally varying bio‐functionality for biodegradable vascular stent applications.