Young exoplanets provide an important link between understanding planet formation and atmospheric evolution1. Direct imaging spectroscopy allows us to infer the properties of young, wide-orbit, giant planets with high signal-to-noise ratio. This allows us to compare this young population with exoplanets characterized by transmission spectroscopy, which has indirectly revealed the presence of clouds2-4, photochemistry5 and a diversity of atmospheric compositions6,7. Direct detections have also been made for brown dwarfs8,9, but direct studies of young giant planets in the mid-infrared were not possible before James Webb Space Telescope10. With two exoplanets around a solar-type star, the YSES-1 system is an ideal laboratory for studying this early phase of exoplanet evolution. Here we report the direct observations of silicate clouds in the atmosphere of the exoplanet YSES-1 c through its 9-11 µm absorption feature, and the first circumplanetary disk silicate emission around its sibling planet, YSES-1 b. The clouds of YSES-1 c are composed of either amorphous iron-enriched pyroxene or a combination of amorphous MgSiO3 and Mg2SiO4, with particle sizes of ≤0.1 μm at 1 millibar pressure. We attribute the emission from the disk around YSES-1 b to be from submicron olivine dust grains, which may have formed through collisions of planet-forming bodies in the disk.

The integrity of the plasma membrane is vital for nearly all aspects of cell functioning1. Mechanical forces can cause plasma membrane damage2, but it is unclear whether there are large molecules that regulate the integrity of the plasma membrane under mechanical strain. Here we constructed a 384-well cellular-stretch system that delivers precise, reproducible strain to cultured cells. Using the system, we screened 10,843 small interfering RNAs (siRNAs) targeting 2,726 multipass transmembrane proteins for strain-induced membrane permeability changes. The screen identified NINJ1-a protein that was recently proposed to regulate pyroptosis and other lytic cell death3,4-as the top hit. We demonstrate that NINJ1 is a critical regulator of mechanical-strain-induced plasma membrane rupture (PMR), without the need for stimulating any cell death programs. NINJ1 levels on the plasma membrane are inversely correlated with the amount of force required to rupture the membrane. In the pyroptosis context, NINJ1 on its own is not sufficient to fully rupture the membrane, and additional mechanical force is required for full PMR. Our study establishes that NINJ1 functions as a bona fide determinant of membrane biomechanical properties. Our study also suggests that PMR across tissues of distinct mechanical microenvironments is subjected to fine-tuning by differences in NINJ1 expression and external forces.