Spin of protoplanets generated by pebble accretion: Influences of protoplanet-induced gas flow

We investigate the spin state of a protoplanet during the pebble accretion influenced by the gas flow in the gravitational potential of the protoplanet and how it depends on the planetary mass, the headwind speed, the distance from the host star, and the pebble size. We perform nonisothermal three-dimensional hydrodynamical simulations in a local frame to obtain the gas flow around the planet. We then numerically integrate three-dimensional orbits of pebbles under the obtained gas flow. Finally, assuming uniform spatial distribution of incoming pebbles, we calculate net spin by summing up specific angular momentum that individual pebbles transfer to the protoplanet at impacts. We find that a protoplanet with the envelope acquires prograde net spin rotation regardless of the planetary mass, the pebble size, and the headwind speed of the gas. This is because accreting pebbles are dragged by the envelope that commonly has prograde rotation. As the planetary mass or orbital radius increases, the envelope is thicker and the prograde rotation is faster, resulting in faster net prograde spin. When the dimensionless thermal mass of the planet, $m = R_{\mathrm{Bondi}} / H$, where $R_{\mathrm{Bondi}}$ and $H$ are the Bondi radius and the disk gas scale height, is larger than a certain critical mass ($m \gtrsim 0.3$ at $0.1 \, \mathrm{au}$ or $m \gtrsim 0.1$ at $1 \, \mathrm{au}$), the spin rotation exceeds the breakup one. The predicted spin frequency reaches the breakup one at the planetary mass $m_{\mathrm{iso,rot}} \sim 0.1 \, (a / 1 \, \mathrm{au})^{-1/2}$ (where $a$ is the orbital radius), suggesting that the protoplanet cannot grow beyond $m_{\mathrm{iso,rot}}$. It is consistent with the Earth's current mass and could help the formation of the Moon by a giant impact on fast-spinning proto-Earth.Comment: 14 pages, 10 figures, Accepted for publication in Astronomy and Astrophysics (A&A

TRAF6 Establishes Innate Immune Responses by Activating NF-κB and IRF7 upon Sensing Cytosolic Viral RNA and DNA

BACKGROUND:In response to viral infection, the innate immune system recognizes viral nucleic acids and then induces production of proinflammatory cytokines and type I interferons (IFNs). Toll-like receptor 7 (TLR7) and TLR9 detect viral RNA and DNA, respectively, in endosomal compartments, leading to the activation of nuclear factor kappaB (NF-kappaB) and IFN regulatory factors (IRFs) in plasmacytoid dendritic cells. During such TLR signaling, TNF receptor-associated factor 6 (TRAF6) is essential for the activation of NF-kappaB and the production of type I IFN. In contrast, RIG-like helicases (RLHs), cytosolic RNA sensors, are indispensable for antiviral responses in conventional dendritic cells, macrophages, and fibroblasts. However, the contribution of TRAF6 to the detection of cytosolic viral nucleic acids has been controversial, and the involvement of TRAF6 in IRF activation has not been adequately addressed. PRINCIPAL FINDINGS:Here we first show that TRAF6 plays a critical role in RLH signaling. The absence of TRAF6 resulted in enhanced viral replication and a significant reduction in the production of IL-6 and type I IFNs after infection with RNA virus. Activation of NF-kappaB and IRF7, but not that of IRF3, was significantly impaired during RLH signaling in the absence of TRAF6. TGFbeta-activated kinase 1 (TAK1) and MEKK3, whose activation by TRAF6 during TLR signaling is involved in NF-kappaB activation, were not essential for RLH-mediated NF-kappaB activation. We also demonstrate that TRAF6-deficiency impaired cytosolic DNA-induced antiviral responses, and this impairment was due to defective activation of NF-kappaB and IRF7. CONCLUSIONS/SIGNIFICANCE:Thus, TRAF6 mediates antiviral responses triggered by cytosolic viral DNA and RNA in a way that differs from that associated with TLR signaling. Given its essential role in signaling by various receptors involved in the acquired immune system, TRAF6 represents a key molecule in innate and antigen-specific immune responses against viral infection