In this research, we propose a new 3D object detector with a trustworthy depth estimation, dubbed BEVDepth, for camera-based Bird's-Eye-View~(BEV) 3D object detection. Our work is based on a key observation -- depth estimation in recent approaches is surprisingly inadequate given the fact that depth is essential to camera 3D detection. Our BEVDepth resolves this by leveraging explicit depth supervision. A camera-awareness depth estimation module is also introduced to facilitate the depth predicting capability. Besides, we design a novel Depth Refinement Module to counter the side effects carried by imprecise feature unprojection. Aided by customized Efficient Voxel Pooling and multi-frame mechanism, BEVDepth achieves the new state-of-the-art 60.9% NDS on the challenging nuScenes test set while maintaining high efficiency. For the first time, the NDS score of a camera model reaches 60%. Codes have been released.

In this paper, we propose a robust 3D detector, named Cross Modal Transformer (CMT), for end-to-end 3D multi-modal detection. Without explicit view transformation, CMT takes the image and point clouds tokens as inputs and directly outputs accurate 3D bounding boxes. The spatial alignment of multi-modal tokens is performed by encoding the 3D points into multi-modal features. The core design of CMT is quite simple while its performance is impressive. It achieves 74.1% NDS (state-of-the-art with single model) on nuScenes test set while maintaining faster inference speed. Moreover, CMT has a strong robustness even if the LiDAR is missing. Code is released at https://github.com/junjie18/CMT.

Cilia are microtubule-based organelles that mediate signal transduction in a variety of tissues. Despite their importance, the signalling cascades that regulate cilium formation remain incompletely understood. Here we report that prostaglandin signalling affects ciliogenesis by regulating anterograde intraflagellar transport (IFT). Zebrafish leakytail (lkt) mutants show ciliogenesis defects, and the lkt locus encodes an ATP-binding cassette transporter (ABCC4). We show that Lkt/ABCC4 localizes to the cell membrane and exports prostaglandin E₂ (PGE₂), a function that is abrogated by the Lkt/ABCC4^T804M mutant. PGE₂ synthesis enzyme cyclooxygenase-1 and its receptor, EP4, which localizes to the cilium and activates the cyclic-AMP-mediated signalling cascade, are required for cilium formation and elongation. Importantly, PGE₂ signalling increases anterograde but not retrograde velocity of IFT and promotes ciliogenesis in mammalian cells. These findings lead us to propose that Lkt/ABCC4-mediated PGE₂ signalling acts through a ciliary G-protein-coupled receptor, EP4, to upregulate cAMP synthesis and increase anterograde IFT, thereby promoting ciliogenesis.

Heart regeneration occurs by dedifferentiation and proliferation of pre-existing cardiomyocytes (CMs). However, the signaling mechanisms by which injury induces CM renewal remain incompletely understood. Here, we find that cardiac injury in zebrafish induces expression of the secreted Wnt inhibitors, including Dickkopf 1 (Dkk1), Dkk3, secreted Frizzled-related protein 1 (sFrp1), and sFrp2, in cardiac tissue adjacent to injury sites. Experimental blocking of Wnt activity via Dkk1 overexpression enhances CM proliferation and heart regeneration, whereas ectopic activation of Wnt8 signaling blunts injury-induced CM dedifferentiation and proliferation. Although Wnt signaling is dampened upon injury, the cytoplasmic β-catenin is unexpectedly increased at disarrayed CM sarcomeres in myocardial wound edges. Our analyses indicated that p21-activated kinase 2 (Pak2) is induced at regenerating CMs, where it phosphorylates cytoplasmic β-catenin at Ser 675 and increases its stability at disassembled sarcomeres. Myocardial-specific induction of the phospho-mimetic β-catenin (S675E) enhances CM dedifferentiation and sarcomere disassembly in response to injury. Conversely, inactivation of Pak2 kinase activity reduces the Ser 675-phosphorylated β-catenin (pS675-β-catenin) and attenuates CM sarcomere disorganization and dedifferentiation. Taken together, these findings demonstrate that coordination of Wnt signaling inhibition and Pak2/pS675-β-catenin signaling enhances zebrafish heart regeneration by supporting CM dedifferentiation and proliferation.