Impact of Atmospheric and Oceanic Conditions on the Frequency and Genesis Location of Tropical Cyclones over the Western North Pacific in 2004 and 2010

This study examines the impact of atmospheric and oceanic conditions during May–August of 2004 and 2010 on the frequency and genesis location of tropical cyclones over the western North Pacific. Using the WRF model, four numerical experiments were carried out based on different atmospheric conditions and SST forcing. The numerical experiments indicated that changes in atmospheric and oceanic conditions greatly affect tropical cyclone activity, and the roles of atmospheric conditions are slightly greater than oceanic conditions. Specifically, the total number of tropical cyclones was found to be mostly affected by atmospheric conditions, while the distribution of tropical cyclone genesis locations was mainly related to oceanic conditions, especially the distribution of SST. In 2010, a warmer SST occurred west of 140°E, with a colder SST east of 140°E. On the one hand, the easterly flow was enhanced through the effect of the increase in the zonal SST gradient.The strengthened easterly flow led to an anomalous boundary layer divergence over the region to the east of 140°E, which suppressed the formation of tropical cyclones over this region. On the other hand, the colder SST over the region to the east of 140°E led to a colder low-level air temperature, which resulted in decreased CAPE and static instability energy. The decrease in thermodynamic energy restricted the generation of tropical cyclones over the same region.

Distinct functions of TiR1 and AFB1 receptors in auxin signaling

Dear Editor,Auxin is the major plant hormone regulating growth and development(Friml,2022).Forward genetic approaches have identified major components of auxin signaling and established the canonical mechanism mediating transcriptional and thus developmental reprogramming in Arabidopsis thaliana.In this textbook view,TRANSPORT INHIBITOR RESPONSE 1(TIR1)/AUXIN-SIGNALING F-BOX(AFB)proteins are auxin receptors,which act as F-box subunits determining the substrate specificity of the Skp1-Cullin1-F box protein(SCF)type E3 ubiquitin ligase complex.Auxin acts as a"molecular glue,"increasing the affinity between TIR1/AFBs and the Auxin/lndole-3-Acetic Acid(Aux/IAA)repressors.Subsequently,Aux/IAAs are ubiquitinated and degraded,thus releasing auxin transcription factors from their repression and making them free to mediate transcription of auxin response genes(Yu et al.,2022).

PD1^+CCR2^+CD8^+T Cells Infiltrate the Central Nervous System during Acute Japanese Encephalitis Virus Infection

Japanese encephalitis(JE)is a viral encephalitis disease caused by Japanese encephalitis virus(JEV)infection.Uncontrolled inflammatory responses in the central nervous system(CNS)are a hallmark of severe JE.Although the CCR2-CCL2 axis is important for monocytes trafficking during JEV infection,little is known about its role in CNS trafficking of CD8^+T cells.Here,we characterized a mouse model of JEV infection,induced via intravenous injection(i.v.)and delineated the chemokines and infiltrating peripheral immune cells in the brains of infected mice.The CNS expression of chemokines,Ccl2,Ccl3,and Ccl5,and their receptors,Ccr2 or Ccr5.was significantly up-regulated after JEV infection and was associated with the degree of JE pathogenesis.Moreover,JEV infection resulted in the migration of a large number of CD8^+T cells into the CNS.In the brains of JEV-infected mice,infiltrating CD8^+T cells expressed CCR2 and CCR5 and were found to comprise mainly effector T cells(CD44^+CD62L_).JEV infection dramatically enhanced the expression of programmed death 1(PD-1)on infiltrating CD8^+T cells in the brain,as compared to that on peripheral CD8^+T cells in the spleen.This effect was more pronounced on infiltrating CCR2^+CD8^+T cells than on CCR2-CD8^+T cells.In conclusion,we identified a new subset of CD8^+T cells(PD1^+CCR2^+CD8^+T cells)present in the CNS of mice during acute JEV infection.These CD8^+T cells might play a role in JE pathogenesis.