中国妖水螨亚科新纪录及佯软滑水螨属二新种(蜱螨亚纲:湿螨总科:软滑水螨科)(英)

报道采自贵州的我国软滑水螨科(Pionidae)之新纪录妖水螨亚科(Tiphyinae)、佯软滑水螨属(Pionopsis)和佯软滑水螨亚属(Pionopsis),并描述该属二新种。 赵氏佯软滑水螨Pionopsis(s. s. )zhaoi Jin et Wiles, sp. nov. (图1 A-F) 正模♂,片号78-1,July11, 1992,贵州省贵阳市花溪河。副模2♂♂,片号78-2、78-3、1♀,片号78-5,采集记录同正模;1♂,片号59-1,1♀,瓶号29,Feb.7,1991,采地同正模,溪流。均金道超采。 本新种近似于沼泽佯软滑水螨Pionopsis(s. s. )paludis Habeeb 1954,但本新种两性背面具背片、雄螨Ⅳ基节板与生殖域愈合、雌螨后基节板群中距非常宽等特征极易与之区别。 长肋佯软滑水螨Pionopsis(s. s. )longicosta Jin et Wiles, sp. nov.(图2A-E) 正模♀,片号78-4,July11,1992,贵州省贵阳市花溪,河,金道超采。 本新种以Ⅳ基节板极发达并具长后突、后基节板群中距狭窄和须肢粗短型等特征显著别于本属所有的10种已知种。     

Effect of adrenocorticotropin fragments on the memory of Tenebrio molitor beetles

Fragments of the adrenocorticotropic hormone ACTH1-24 and ACTH5-7 facilitate memory in the beetle T. molitor, the effect being observed at different stages after learning. An analogue of ACTH5-7 which contains D-phenylalamine, as well as D-phen7-ACTH4-7, inhibit memorization (the results checked 1 day after learning) and induce some other disturbances in the behaviour of beetles. To the 10th day of learning, the effects of the analogues cannot be distinguished from those of L-Phe7-fragments. The results obtained are compared with the known effect of ACTH fragments on memory in vertebrates.     

Cytosolic acidification precedes nitric oxide removal during inhibition of ABA-induced stomatal closure by fusicoccin

The role of nitric oxide (NO) and the relationship between NO and cytosolic pH during inhibition of ABA effect by fusicoccin (FC) in guard cells of Vicia faba were analyzed. ABA induced NO generation and stomatal closure, but FC inhibited the effects of ABA. Treatment with 2-(4-carboxyphenyl)-4,4,5,5-tetra-methylimidazoline-1-oxyl-3-oxide (cPTIO) and N^G-nitro-L-Arg-methyl ester (L-NAME) mimicked the effects of FC. These data suggest that inhibition of ABA effect by FC is possibly related to the decreasing in the NO level. Furthermore, like cPTIO, FC not only suppressed stomatal closure and NO level in guard cells treated with NO donor sodium nitroprusside (SNP), but also reopened stomata, which had been closed by ABA, and reduced the level of NO in guard cells that had been produced by ABA, indicating that FC caused NO removal. Butyric acid simulated the effects of FC on the stomatal aperture and increased NO levels in guard cells treated with SNP and had been closed by ABA, and both FC and butyric acid surely reduced cytosolic pH, which demonstrates that cytosolic acidification mediates FC-induced NO removal. Taken together, our results show that FC induces NO removal and reduces NO level via cytosolic acidification in guard cells, thus inhibiting ABA effect.     

Quinolinones Alkaloids with AChE Inhibitory Activity from Mangrove Endophytic Fungus Penicillium citrinum YX-002

Acetylcholinesterase (AChE) inhibitory activity-guided studies on the mangrove-derived endophytic fungus Penicillium citrinum YX-002 led to the isolation of nine secondary metabolites, including one new quinolinone derivative, quinolactone A ( 1 ), a pair of epimers quinolactacin C1 ( 2 ) and 3-epi-quinolactacin C1 ( 3 ), together with six known analogs ( 4 – 9 ). Their structures were elucidated based on extensive mass spectrometry (MS) and 1D/2D nuclear magnetic resonance (NMR) spectroscopic analyses, and compared with data in the literature. The absolute configurations of compounds 1 – 3 was determined by combination of electronic circular dichroism (ECD) calculations and X-Ray single crystal diffraction technique using CuK_α radiation. In bioassays, compounds 1 , 4 and 7 showed moderate AChE inhibitory activities with IC₅₀ values of 27.6, 19.4 and 11.2 μmol/L, respectively. The structure-activity relationships (SARs) analysis suggested that the existence of carbonyl group on C-3 and the oxygen atom on the five-membered ring were beneficial to the activity. Molecular docking results showed that compound 7 had a lower affinity interaction energy (−9.3 kcal/mol) with stronger interactions with different sites in AChE activities, which explained its higher activities.     

Zika virus elicits inflammation to evade antiviral response by cleaving cGAS via NS1‐caspase‐1 axis

Viral infection triggers host innate immune responses, which primarily include the activation of type I interferon (IFN) signaling and inflammasomes. Here, we report that Zika virus (ZIKV) infection triggers NLRP3 inflammasome activation, which is further enhanced by viral non‐structural protein NS1 to benefit its replication. NS1 recruits the host deubiquitinase USP8 to cleave K11‐linked poly‐ubiquitin chains from caspase‐1 at Lys134, thus inhibiting the proteasomal degradation of caspase‐1. The enhanced stabilization of caspase‐1 by NS1 promotes the cleavage of cGAS, which recognizes mitochondrial DNA release and initiates type I IFN signaling during ZIKV infection. NLRP3 deficiency increases type I IFN production and strengthens host resistance to ZIKVin vitro and in vivo. Taken together, our work unravels a novel antagonistic mechanism employed by ZIKV to suppress host immune response by manipulating the interplay between inflammasome and type I IFN signaling, which might guide the rational design of therapeutics in the future.