The Golgi apparatus is a membrane-bounded organelle with the characteristic shape of a series of stacked flat cisternae. During mitosis in mammalian cells, the Golgi apparatus is once fragmented into small vesicles and then reassembled to form the characteristic shape again in each daughter cell. The mechanism and details of the reassembly process remain elusive. Here, by the physical simulation of a coarse-grained membrane model, we reconstructed the threedimensional morphological dynamics of the Golgi reassembly process. Considering the stability of the interphase Golgi shape, we introduce two hypothetical mechanisms-the Golgi rim stabilizer protein and curvature-dependent restriction on membrane fusioninto the general biomembrane model. We show that the characteristic Golgi shape is spontaneously organized from the assembly of vesicles by proper tuning of the two additional mechanisms, i.e., the Golgi reassembly process is modeled as self-organization. We also demonstrate that the fine Golgi shape forms via a balance of three reaction speeds: vesicle aggregation, membrane fusion, and shape relaxation. Moreover, the membrane fusion activity decreases thickness and the number of stacked cisternae of the emerging shapes.Golgi apparatus | self-organization | physical biology modeling | computer simulation

Summary Autophagy is an intracellular degradation process that is mediated by de novo formation of autophagosomes. Autophagosome formation involves dynamic morphological changes; a disk-shaped membrane cisterna grows, bends to become a cup-shaped structure, and finally develops into a spherical autophagosome. We have constructed a theoretical model that integrates the membrane morphological change and entropic partitioning of putative curvature generators, which we have used to investigate the autophagosome formation process quantitatively. We show that the membrane curvature and the distribution of the curvature generators stabilize disk- and cup-shaped intermediate structures during autophagosome formation, which is quantitatively consistent with in vivo observations. These results suggest that various autophagy proteins with membrane curvature-sensing properties control morphological change by stabilizing these intermediate structures. Our model provides a framework for understanding autophagosome formation.

Context. Regular observations of Jupiter by a large number of amateur astronomers have resulted in the serendipitous discovery of short bright flashes in its atmosphere, which have been proposed as being caused by impacts of small objects. Three flashes were detected: one on June 3, 2010, one on August 20, 2010, and one on September 10, 2012. Aims. We show that the flashes are caused by impacting objects that we characterize in terms of their size, and we study the flux of small impacts on Jupiter. Methods. We measured the light curves of these atmospheric airbursts to extract their luminous energy and computed the masses and sizes of the objects. We ran simulations of impacts and compared them with the light curves. We analyzed the statistical significance of these events in the large pool of Jupiter observations. Results. All three objects are in the 5−20 m size category depending on their density, and they released energy comparable to the recent Chelyabinsk airburst. Model simulations approximately agree with the interpretation of the limited observations. Biases in observations of Jupiter suggest a rate of 12−60 similar impacts per year and we provide software tools for amateurs to examine the faint signature of impacts in their data to increase the number of detected collisions. Conclusions. The impact rate agrees with dynamical models of comets. More massive objects (a few 100 m) should impact with Jupiter every few years leaving atmospheric dark debris features that could be detectable about once per decade.