Learning Controllable 3D Diffusion Models from Single-view Images

Diffusion models have recently become the de-facto approach for generative modeling in the 2D domain. However, extending diffusion models to 3D is challenging due to the difficulties in acquiring 3D ground truth data for training. On the other hand, 3D GANs that integrate implicit 3D representations into GANs have shown remarkable 3D-aware generation when trained only on single-view image datasets. However, 3D GANs do not provide straightforward ways to precisely control image synthesis. To address these challenges, We present Control3Diff, a 3D diffusion model that combines the strengths of diffusion models and 3D GANs for versatile, controllable 3D-aware image synthesis for single-view datasets. Control3Diff explicitly models the underlying latent distribution (optionally conditioned on external inputs), thus enabling direct control during the diffusion process. Moreover, our approach is general and applicable to any type of controlling input, allowing us to train it with the same diffusion objective without any auxiliary supervision. We validate the efficacy of Control3Diff on standard image generation benchmarks, including FFHQ, AFHQ, and ShapeNet, using various conditioning inputs such as images, sketches, and text prompts. Please see the project website (\url{https://jiataogu.me/control3diff}) for video comparisons.Comment: work in progres

Regulation of jasmonate signaling by reversible acetylation of TOPLESS in Arabidopsis

The plant hormone jasmonate regulates plant immunity and adaptive growth through orchestrating a genome-wide transcriptional program. Key regulators of jasmonate-responsive gene expression include the master transcription factor MYC2, which are repressed by the conserved Groucho/Tup1-like co-repressor TOPLESS (TPL) in the resting state. However, the mechanisms underlying TPL-mediated transcriptional repression of MYC2 activity and hormone-dependent switching between repression and de-repression remain enigmatic. Here, we report the regulation of TPL activity through reversible TPL acetylation. The histone acetyltransferase GCN5 mediates TPL acetylation, which enhances its interaction with the NOVEL-INTERACTOR-OF-JAZ (NINJA) adaptor and promotes its recruitment to MYC2 target promoters, facilitating repression. Conversely, TPL deacetylation by the histone deacetylase HDA6 weakens TPL–NINJA interaction and inhibits TPL recruitment to MYC2 target promoters, facilitating activation. In a resting state, the opposing activities of GCN5 and HDA6 maintain TPL acetylation homeostasis, promoting TPL repression activity. In response to jasmonate elicitation, HAD6 expression is transiently induced, decreasing TPL acetylation and repressor activity, facilitating target gene activation. Thus, the GCN5–TPL–HDA6 module maintains the homeostasis of acetylated TPL, thereby determining the transcriptional state of jasmonate-responsive genes. Our findings uncovered a mechanism by which the TPL co-repressor activity in jasmonate signaling being actively tuned in a rapid and reversible manner

A Jasmonate Signaling Network Activates Root Stem Cells and Promotes Regeneration

Plants are sessile and have to cope with environmentally induced damage through modification of growth and defense pathways. How tissue regeneration is triggered in such responses and whether this involves stem cell activation is an open question. The stress hormone jasmonate (JA) plays well-established roles in wounding and defense responses. JA also affects growth, which is hitherto interpreted as a trade-off between growth and defense. Here, we describe a molecular network triggered by wound-induced JA that promotes stem cell activation and regeneration. JA regulates organizer cell activity in the root stem cell niche through the RBR-SCR network and stress response protein ERF115. Moreover, JA-induced ERF109 transcription stimulates CYCD6;1 expression, functions upstream of ERF115, and promotes regeneration. Soil penetration and response to nematode herbivory induce and require this JA-mediated regeneration response. Therefore, the JA tissue damage response pathway induces stem cell activation and regeneration and activates growth after environmental stress

Bestatin, an Inhibitor of Aminopeptidases, Provides a Chemical Genetics Approach to Dissect Jasmonate Signaling in Arabidopsis

Bestatin, a potent inhibitor of some aminopeptidases, was shown previously to be a powerful inducer of wound-response genes in tomato (Lycopersicon esculentum). Here, we present several lines of evidence showing that bestatin specifically activates jasmonic acid (JA) signaling in plants. First, bestatin specifically activates the expression of JA-inducible genes in tomato and Arabidopsis (Arabidopsis thaliana). Second, the induction of JA-responsive genes by bestatin requires the COI1-dependent JA-signaling pathway, but does not depend strictly on JA biosynthesis. Third, microarray analysis using Arabidopsis whole-genome chip demonstrates that the gene expression profile of bestatin-treated plants is similar to that of JA-treated plants. Fourth, bestatin promotes a series of JA-related developmental phenotypes. Taken together, the unique action mode of bestatin in regulating JA-signaled processes leads us to the hypothesis that bestatin exerts its effects through the modulation of some key regulators in JA signaling. We have employed bestatin as an experimental tool to dissect JA signaling through a chemical genetic screening, which yielded a collection of Arabidopsis bestatin-resistant (ber) mutants that are insensitive to the inhibitory effects of bestatin on root elongation. Further characterization efforts demonstrate that some ber mutants are defective in various JA-induced responses, which allowed us to classify the ber mutants into three phenotypic groups: JA-insensitive ber mutants, JA-hypersensitive ber mutants, and mutants insensitive to bestatin but showing normal response to JA. Genetic and phenotypic analyses of the ber mutants with altered JA responses indicate that we have identified several novel loci involved in JA signaling