A process-based model reveals the restoration gap of degraded grasslands in Inner Mongolian steppe.

Due to the influence of climate change and extensive grazing, a large proportion of steppe grassland has been degraded worldwide. The Chinese government initiated a series of grassland restoration programs to reverse the degradation. However, the limiting factors and the restoration potential remain unknown. Here we present a process-based model to assess the restoration gap (RG) defined as maximum biomass differences between non-degraded and degraded grasslands with different degrees of soil and vegetation degradation. The process-based model Agricultural Production Systems Simulator (APSIM) was evaluated utilizing observation data from both typical and meadow steppes under natural conditions in terms of phenology, dynamics of above-ground biomass and soil water content. Scenario analysis and sensitivity analysis were subsequently performed to address the RG and controlling factors during 1969-2018. The results showed that the calibrated model performed well with r > 0.75 and model efficiency factor EF > 0.5 for all the simulation components. According to our model results, the RG was larger in typical steppe compared to that of meadow steppe and it increased with increasing soil and/or vegetation degradation, to ~60% under extremely degraded scenarios. Both soil and vegetation degradation led to reduced water use efficiency, with an elevated proportion of soil evaporation to evapotranspiration (Es/ET), however, the limiting factor for RG varied. The degradation of soil water holding capacity contributed more to RG regardless of climate conditions for typical steppe in all years and for meadow steppe in dry years. In wet years the importance of vegetation coverage reduction increased for RG in meadow steppe, where the relative importance of vegetation coverage (valued at 62.8%) was 25.6% higher than that of soil degradation. Our results demonstrated the importance of considering climate variations when developing protection and restoration programs for grassland ecosystems.

A natural symbiotic bacterium drives mosquito refractoriness to Plasmodium infection via secretion of an antimalarial lipase.

The stalling global progress in the fight against malaria prompts the urgent need to develop new intervention strategies. Whilst engineered symbiotic bacteria have been shown to confer mosquito resistance to parasite infection, a major challenge for field implementation is to address regulatory concerns. Here, we report the identification of a Plasmodium-blocking symbiotic bacterium, Serratia ureilytica Su_YN1, isolated from the midgut of wild Anopheles sinensis in China that inhibits malaria parasites via secretion of an antimalarial lipase. Analysis of Plasmodium vivax epidemic data indicates that local malaria cases in Tengchong (Yunnan province, China) are significantly lower than imported cases and importantly, that the local vector A. sinensis is more resistant to infection by P. vivax than A. sinensis from other regions. Analysis of the gut symbiotic bacteria of mosquitoes from Yunnan province led to the identification of S. ureilytica Su_YN1. This bacterium renders mosquitoes resistant to infection by the human parasite Plasmodium falciparum or the rodent parasite Plasmodium berghei via secretion of a lipase that selectively kills parasites at various stages. Importantly, Su_YN1 rapidly disseminates through mosquito populations by vertical and horizontal transmission, providing a potential tool for blocking malaria transmission in the field.

The Zscan4-Tet2 Transcription Nexus Regulates Metabolic Rewiring and Enhances Proteostasis to Promote Reprogramming.

Evolutionarily conserved SCAN (named after SRE-ZBP, CTfin51, AW-1, and Number 18 cDNA)-domain-containing zinc finger transcription factors (ZSCAN) have been found in both mouse and human genomes. Zscan4 is transiently expressed during zygotic genome activation (ZGA) in preimplantation embryos and induced pluripotent stem cell (iPSC) reprogramming. However, little is known about the mechanism of Zscan4 underlying these processes of cell fate control. Here, we show that Zscan4f, a representative of ZSCAN proteins, is able to recruit Tet2 through its SCAN domain. The Zscan4f-Tet2 interaction promotes DNA demethylation and regulates the expression of target genes, particularly those encoding glycolytic enzymes and proteasome subunits. Zscan4f regulates metabolic rewiring, enhances proteasome function, and ultimately promotes iPSC generation. These results identify Zscan4f as an important partner of Tet2 in regulating target genes and promoting iPSC generation and suggest a possible and common mechanism shared by SCAN family transcription factors to recruit ten-eleven translocation (TET) DNA dioxygenases to regulate diverse cellular processes, including reprogramming.