Catch me if you can – the crosstalk of ZIKV and the restriction factor Tetherin

Zika virus (ZIKV) is a flavivirus that is mainly transmitted by Aedes mosquitos and normally causes mild symptoms. During the outbreak in the Americas in 2015, it was associated with more severe implications, like microcephaly in new-borns and the Gullain-Barré syndrome. The lack of specific vaccines and cures strengthen the need for a deeper understanding of the virus life cycle and virus-host interactions. The restriction factor tetherin (THN) is an interferon-inducible cellular protein with broad antiviral properties. It is known to inhibit the release of various enveloped viruses by tethering them to each other and to the cell membrane, thereby preventing their further spread. On the other hand, different viruses have developed various escape strategies against THN. Analysis of the crosstalk between ZIKV and THN revealed that in spite of a strong induction of THN mRNA expression in ZIKV-infected cells, this is not reflected by an elevated protein level of THN. Contrariwise, the THN protein level is decreased due to a reduced half-life. The increased degradation of THN in ZIKV infected cells involves the endo-lysosomal system, but does not depend on the early steps of autophagy. Enrichment of THN by depletion of the ESCRT-0 protein HRS diminishes ZIKV release and spread, which points out the capacity of THN to restrict ZIKV and explains the enhanced THN degradation in infected cells as an effective viral escape strategy. Importance Although tetherin expression is strongly induced by ZIKV infection there is a reduction in the amount of tetherin protein. This is due to an enhanced lysosomal degradation. However, if tetherin level is rescued release of ZIKV is impaired. This shows that tetherin is a restriction factor for ZIKV and the induction of an efficient degradation represents a viral escape strategy. To our knowledge this is the first study that describes and characterizes tetherin as an restriction factor for ZIKV life cycle.

Metabolite and Phytohormone Profiling Illustrates Metabolic Reprogramming as an Escape Strategy of Deepwater Rice during Partially Submerged Stress

Rice varieties that can survive under submergence conditions respond to flooding either by enhancing internode elongation or by quiescence of shoot elongation. Despite extensive efforts to identify key metabolites triggered by complete submergence of rice possessing SUBMERGENCE 1 (SUB1) locus, metabolic responses of internode elongation of deepwater rice governed by the SNORKEL 1 and 2 genes remain elusive. This study investigated specific metabolomic responses under partial submergence (PS) to deepwater- (C9285) and non-deepwater rice cultivars (Taichung 65 (T65)). In addition, we examined the response in a near-isogenic line (NIL-12) that has a C9285 genomic fragment on chromosome 12 introgressed into the genetic background of T65. Under short-term submergence (0–24 h), metabolite profiles of C9285, NIL-12, and T65 were compared to extract significantly changed metabolites in deepwater rice under PS conditions. Comprehensive metabolite and phytohormone profiling revealed increases in metabolite levels in the glycolysis pathway in NIL-12 plants. Under long-term submergence (0–288 h), we found decreased amino acid levels. These metabolomic changes were opposite when compared to those in flood-tolerant rice with SUB1 locus. Auxin conjugate levels related to stress response decreased in NIL-12 lines relative to T65. Our analysis helped clarify the complex metabolic reprogramming in deepwater rice as an escape strategy.

Flagellum malfunctions trigger metaboly as an escape strategy in Euglena gracilis

Euglenoids, a family of aquatic unicellular organisms, present the ability to alter the shape of their bodies, a process referred to as metaboly [1–5]. Metaboly is usually used by phagotrophic cells to engulf their prey. However, Euglena gracilis is osmotrophic and photosynthetic. Though metaboly was discovered centuries ago, it remains unclear why E. gracilis undergo metaboly and what causes them to deform [1–5], and some consider metaboly to be a functionless ancestral vestige [5]. Here, we show that flagellum malfunctions trigger metaboly and metaboly is an escape strategy adopted by E. gracilis when the proper rotation and beating of the flagellum are hindered by restrictions including surface obstruction, sticking, resistance, or limited space. Metaboly facilitates escape in five ways: 1) detaching the body from the surface and decreasing the attaching area attached to the interface, which decreases the adhering force and is advantageous for escaping; 2) enlarging the space between flagellum and the restricting surface which restores beating and rotation of the flagellum; 3) decreasing the torque of viscous resistance for rotation of the body and changing the direction of the body to restore flagellar function; 4) decreasing the length of the body, which pulls the flagellum away from the restrictive situations; and 5) crawling backwards on a surface or swimming backwards in a bulk fluid if the flagellum completely malfunctions or has broken off. Taken together, our findings suggest that metaboly plays a key role in enabling E. gracilis to escape from harmful conditions when flagellar functions is impaired or absent. Our findings can inspire the bionic design of adaptive soft robots and facilitate the control of water blooms of euglena in freshwater aquiculture industry.