TY - JOUR AB - We present a unified framework tackling two problems: class-specific 3D reconstruction from a single image, and generation of new 3D shape samples. These tasks have received considerable attention recently; however, most existing approaches rely on 3D supervision, annotation of 2D images with keypoints or poses, and/or training with multiple views of each object instance. Our framework is very general: it can be trained in similar settings to existing approaches, while also supporting weaker supervision. Importantly, it can be trained purely from 2D images, without pose annotations, and with only a single view per instance. We employ meshes as an output representation, instead of voxels used in most prior work. This allows us to reason over lighting parameters and exploit shading information during training, which previous 2D-supervised methods cannot. Thus, our method can learn to generate and reconstruct concave object classes. We evaluate our approach in various settings, showing that: (i) it learns to disentangle shape from pose and lighting; (ii) using shading in the loss improves performance compared to just silhouettes; (iii) when using a standard single white light, our model outperforms state-of-the-art 2D-supervised methods, both with and without pose supervision, thanks to exploiting shading cues; (iv) performance improves further when using multiple coloured lights, even approaching that of state-of-the-art 3D-supervised methods; (v) shapes produced by our model capture smooth surfaces and fine details better than voxel-based approaches; and (vi) our approach supports concave classes such as bathtubs and sofas, which methods based on silhouettes cannot learn. AU - Henderson, Paul M AU - Ferrari, Vittorio ID - 6952 JF - International Journal of Computer Vision SN - 0920-5691 TI - Learning single-image 3D reconstruction by generative modelling of shape, pose and shading VL - 128 ER - TY - JOUR AB - In the cerebellum, GluD2 is exclusively expressed in Purkinje cells, where it regulates synapse formation and regeneration, synaptic plasticity, and motor learning. Delayed cognitive development in humans with GluD2 gene mutations suggests extracerebellar functions of GluD2. However, extracerebellar expression of GluD2 and its relationship with that of GluD1 are poorly understood. GluD2 mRNA and protein were widely detected, with relatively high levels observed in the olfactory glomerular layer, medial prefrontal cortex, cingulate cortex, retrosplenial granular cortex, olfactory tubercle, subiculum, striatum, lateral septum, anterodorsal thalamic nucleus, and arcuate hypothalamic nucleus. These regions were also enriched for GluD1, and many individual neurons coexpressed the two GluDs. In the retrosplenial granular cortex, GluD1 and GluD2 were selectively expressed at PSD‐95‐expressing glutamatergic synapses, and their coexpression on the same synapses was shown by SDS‐digested freeze‐fracture replica labeling. Biochemically, GluD1 and GluD2 formed coimmunoprecipitable complex formation in HEK293T cells and in the cerebral cortex and hippocampus. We further estimated the relative protein amount by quantitative immunoblotting using GluA2/GluD2 and GluA2/GluD1 chimeric proteins as standards for titration of GluD1 and GluD2 antibodies. Intriguingly, the relative amount of GluD2 was almost comparable to that of GluD1 in the postsynaptic density fraction prepared from the cerebral cortex and hippocampus. In contrast, GluD2 was overwhelmingly predominant in the cerebellum. Thus, we have determined the relative extracerebellar expression of GluD1 and GluD2 at regional, neuronal, and synaptic levels. These data provide a molecular–anatomical basis for possible competitive and cooperative interactions of GluD family members at synapses in various brain regions. AU - Nakamoto, Chihiro AU - Konno, Kohtarou AU - Miyazaki, Taisuke AU - Nakatsukasa, Ena AU - Natsume, Rie AU - Abe, Manabu AU - Kawamura, Meiko AU - Fukazawa, Yugo AU - Shigemoto, Ryuichi AU - Yamasaki, Miwako AU - Sakimura, Kenji AU - Watanabe, Masahiko ID - 7148 IS - 6 JF - Journal of Comparative Neurology SN - 0021-9967 TI - Expression mapping, quantification, and complex formation of GluD1 and GluD2 glutamate receptors in adult mouse brain VL - 528 ER - TY - JOUR AB - Removal of the Bax gene from mice completely protects the somas of retinal ganglion cells (RGCs) from apoptosis following optic nerve injury. This makes BAX a promising therapeutic target to prevent neurodegeneration. In this study, Bax+/− mice were used to test the hypothesis that lowering the quantity of BAX in RGCs would delay apoptosis following optic nerve injury. RGCs were damaged by performing optic nerve crush (ONC) and then immunostaining for phospho-cJUN, and quantitative PCR were used to monitor the status of the BAX activation mechanism in the months following injury. The apoptotic susceptibility of injured cells was directly tested by virally introducing GFP-BAX into Bax−/− RGCs after injury. The competency of quiescent RGCs to reactivate their BAX activation mechanism was tested by intravitreal injection of the JNK pathway agonist, anisomycin. Twenty-four weeks after ONC, Bax+/− mice had significantly less cell loss in their RGC layer than Bax+/+ mice 3 weeks after ONC. Bax+/− and Bax+/+ RGCs exhibited similar patterns of nuclear phospho-cJUN accumulation immediately after ONC, which persisted in Bax+/− RGCs for up to 7 weeks before abating. The transcriptional activation of BAX-activating genes was similar in Bax+/− and Bax+/+ RGCs following ONC. Intriguingly, cells deactivated their BAX activation mechanism between 7 and 12 weeks after crush. Introduction of GFP-BAX into Bax−/− cells at 4 weeks after ONC showed that these cells had a nearly normal capacity to activate this protein, but this capacity was lost 8 weeks after crush. Collectively, these data suggest that 8–12 weeks after crush, damaged cells no longer displayed increased susceptibility to BAX activation relative to their naïve counterparts. In this same timeframe, retinal glial activation and the signaling of the pro-apoptotic JNK pathway also abated. Quiescent RGCs did not show a timely reactivation of their JNK pathway following intravitreal injection with anisomycin. These findings demonstrate that lowering the quantity of BAX in RGCs is neuroprotective after acute injury. Damaged RGCs enter a quiescent state months after injury and are no longer responsive to an apoptotic stimulus. Quiescent RGCs will require rejuvenation to reacquire functionality. AU - Donahue, RJ AU - Maes, Margaret E AU - Grosser, JA AU - Nickells, RW ID - 7033 IS - 2 JF - Molecular Neurobiology SN - 0893-7648 TI - BAX-depleted retinal ganglion cells survive and become quiescent following optic nerve damage VL - 57 ER - TY - JOUR AU - Zhang, Yuzhou AU - Friml, Jiří ID - 6997 IS - 3 JF - New Phytologist SN - 0028-646x TI - Auxin guides roots to avoid obstacles during gravitropic growth VL - 225 ER - TY - JOUR AB - In recent years, many genes have been associated with chromatinopathies classified as “Cornelia de Lange Syndrome‐like.” It is known that the phenotype of these patients becomes less recognizable, overlapping to features characteristic of other syndromes caused by genetic variants affecting different regulators of chromatin structure and function. Therefore, Cornelia de Lange syndrome diagnosis might be arduous due to the seldom discordance between unexpected molecular diagnosis and clinical evaluation. Here, we review the molecular features of Cornelia de Lange syndrome, supporting the hypothesis that “CdLS‐like syndromes” are part of a larger “rare disease family” sharing multiple clinical features and common disrupted molecular pathways. AU - Avagliano, Laura AU - Parenti, Ilaria AU - Grazioli, Paolo AU - Di Fede, Elisabetta AU - Parodi, Chiara AU - Mariani, Milena AU - Kaiser, Frank J. AU - Selicorni, Angelo AU - Gervasini, Cristina AU - Massa, Valentina ID - 7149 IS - 1 JF - Clinical Genetics SN - 0009-9163 TI - Chromatinopathies: A focus on Cornelia de Lange syndrome VL - 97 ER - TY - JOUR AB - We define an action of the (double of) Cohomological Hall algebra of Kontsevich and Soibelman on the cohomology of the moduli space of spiked instantons of Nekrasov. We identify this action with the one of the affine Yangian of gl(1). Based on that we derive the vertex algebra at the corner Wr1,r2,r3 of Gaiotto and Rapčák. We conjecture that our approach works for a big class of Calabi–Yau categories, including those associated with toric Calabi–Yau 3-folds. AU - Rapcak, Miroslav AU - Soibelman, Yan AU - Yang, Yaping AU - Zhao, Gufang ID - 7004 JF - Communications in Mathematical Physics SN - 0010-3616 TI - Cohomological Hall algebras, vertex algebras and instantons VL - 376 ER - TY - JOUR AB - Plant root architecture dynamically adapts to various environmental conditions, such as salt‐containing soil. The phytohormone abscisic acid (ABA) is involved among others also in these developmental adaptations, but the underlying molecular mechanism remains elusive. Here, a novel branch of the ABA signaling pathway in Arabidopsis involving PYR/PYL/RCAR (abbreviated as PYLs) receptor‐protein phosphatase 2A (PP2A) complex that acts in parallel to the canonical PYLs‐protein phosphatase 2C (PP2C) mechanism is identified. The PYLs‐PP2A signaling modulates root gravitropism and lateral root formation through regulating phytohormone auxin transport. In optimal conditions, PYLs ABA receptor interacts with the catalytic subunits of PP2A, increasing their phosphatase activity and thus counteracting PINOID (PID) kinase‐mediated phosphorylation of PIN‐FORMED (PIN) auxin transporters. By contrast, in salt and osmotic stress conditions, ABA binds to PYLs, inhibiting the PP2A activity, which leads to increased PIN phosphorylation and consequently modulated directional auxin transport leading to adapted root architecture. This work reveals an adaptive mechanism that may flexibly adjust plant root growth to withstand saline and osmotic stresses. It occurs via the cross‐talk between the stress hormone ABA and the versatile developmental regulator auxin. AU - Li, Yang AU - Wang, Yaping AU - Tan, Shutang AU - Li, Zhen AU - Yuan, Zhi AU - Glanc, Matous AU - Domjan, David AU - Wang, Kai AU - Xuan, Wei AU - Guo, Yan AU - Gong, Zhizhong AU - Friml, Jiří AU - Zhang, Jing ID - 7204 IS - 3 JF - Advanced Science TI - Root growth adaptation is mediated by PYLs ABA receptor-PP2A protein phosphatase complex VL - 7 ER - TY - JOUR AB - BACKGROUND:The introduction of image-guided methods to bypass surgery has resulted in optimized preoperative identification of the recipients and excellent patency rates. However, the recently presented methods have also been resource-consuming. In the present study, we have reported a cost-efficient planning workflow for extracranial-intracranial (EC-IC) revascularization combined with transdural indocyanine green videoangiography (tICG-VA). METHODS:We performed a retrospective review at a single tertiary referral center from 2011 to 2018. A novel software-derived workflow was applied for 25 of 92 bypass procedures during the study period. The precision and accuracy were assessed using tICG-VA identification of the cortical recipients and a comparison of the virtual and actual data. The data from a control group of 25 traditionally planned procedures were also matched. RESULTS:The intraoperative transfer time of the calculated coordinates averaged 0.8 minute (range, 0.4-1.9 minutes). The definitive recipients matched the targeted branches in 80%, and a neighboring branch was used in 16%. Our workflow led to a significant craniotomy size reduction in the study group compared with that in the control group (P = 0.005). tICG-VA was successfully applied in 19 cases. An average of 2 potential recipient arteries were identified transdurally, resulting in tailored durotomy and 3 craniotomy adjustments. Follow-up patency results were available for 49 bypass surgeries, comprising 54 grafts. The overall patency rate was 91% at a median follow-up period of 26 months. No significant difference was found in the patency rate between the study and control groups (P = 0.317). CONCLUSIONS:Our clinical results have validated the presented planning and surgical workflow and support the routine implementation of tICG-VA for recipient identification before durotomy. AU - Dodier, Philippe AU - Auzinger, Thomas AU - Mistelbauer, Gabriel AU - Wang, Wei Te AU - Ferraz-Leite, Heber AU - Gruber, Andreas AU - Marik, Wolfgang AU - Winter, Fabian AU - Fischer, Gerrit AU - Frischer, Josa M. AU - Bavinzski, Gerhard ID - 7220 IS - 2 JF - World Neurosurgery SN - 1878-8750 TI - Novel software-derived workflow in extracranial–intracranial bypass surgery validated by transdural indocyanine green videoangiography VL - 134 ER - TY - JOUR AB - The phytohormone auxin acts as an amazingly versatile coordinator of plant growth and development. With its morphogen-like properties, auxin controls sites and timing of differentiation and/or growth responses both, in quantitative and qualitative terms. Specificity in the auxin response depends largely on distinct modes of signal transmission, by which individual cells perceive and convert auxin signals into a remarkable diversity of responses. The best understood, or so-called canonical mechanism of auxin perception ultimately results in variable adjustments of the cellular transcriptome, via a short, nuclear signal transduction pathway. Additional findings that accumulated over decades implied that an additional, presumably, cell surface-based auxin perception mechanism mediates very rapid cellular responses and decisively contributes to the cell's overall hormonal response. Recent investigations into both, nuclear and cell surface auxin signalling challenged this assumed partition of roles for different auxin signalling pathways and revealed an unexpected complexity in transcriptional and non-transcriptional cellular responses mediated by auxin. AU - Gallei, Michelle C AU - Luschnig, Christian AU - Friml, Jiří ID - 7142 IS - 2 JF - Current Opinion in Plant Biology SN - 1369-5266 TI - Auxin signalling in growth: Schrödinger's cat out of the bag VL - 53 ER - TY - JOUR AB - In the living cell, we encounter a large variety of motile processes such as organelle transport and cytoskeleton remodeling. These processes are driven by motor proteins that generate force by transducing chemical free energy into mechanical work. In many cases, the molecular motors work in teams to collectively generate larger forces. Recent optical trapping experiments on small teams of cytoskeletal motors indicated that the collectively generated force increases with the size of the motor team but that this increase depends on the motor type and on whether the motors are studied in vitro or in vivo. Here, we use the theory of stochastic processes to describe the motion of N motors in a stationary optical trap and to compute the N-dependence of the collectively generated forces. We consider six distinct motor types, two kinesins, two dyneins, and two myosins. We show that the force increases always linearly with N but with a prefactor that depends on the performance of the single motor. Surprisingly, this prefactor increases for weaker motors with a lower stall force. This counter-intuitive behavior reflects the increased probability with which stronger motors detach from the filament during strain generation. Our theoretical results are in quantitative agreement with experimental data on small teams of kinesin-1 motors. AU - Ucar, Mehmet C AU - Lipowsky, Reinhard ID - 7166 IS - 1 JF - Nano Letters SN - 1530-6984 TI - Collective force generation by molecular motors is determined by strain-induced unbinding VL - 20 ER -