An updated phylogeny and adaptive evolution within Amaranthaceae s.l. inferred from multiple phylogenomic datasets.

Amaranthaceae s.l. is a widely distributed family consisting of over 170 genera and 2000 species. Previous molecular phylogenetic studies have shown that Amaranthaceae s.s. and traditional Chenopodiaceae form a monophyletic group (Amaranthaceae s.l.), however, the relationships within this evolutionary branch have yet to be fully resolved. In this study, we assembled the complete plastomes and full-length ITS of 21 Amaranthaceae s.l. individuals and compared them with 38 species of Amaranthaceae s.l. Through plastome structure and sequence alignment analysis, we identified a reverse complementary region approximately 5200 bp long in the genera Atriplex and Chenopodium. Adaptive evolution analysis revealed significant positive selection in eight genes, which likely played a driving role in the evolution of Amaranthaceae s.l., as demonstrated by partitioned evolutionary analysis. Furthermore, we found that about two-thirds of the examined species lack the ycf15 gene, potentially associated with natural selection pressures from their adapted habitats. The phylogenetic tree indicated that some genera (Chenopodium, Halogeton, and Subtr. Salsolinae) are paraphyletic lineages. Our results strongly support the clustering of Amaranthaceae s.l. with monophyletic traditional Chenopodiaceae (Clades I and II) and Amaranthaceae s.s. After a comprehensive analysis, we determined that cytonuclear conflict, gene selection by adapted habitats, and incomplete lineage sorting (ILS) events were the primary reasons for the inconsistent phylogeny of Amaranthaceae s.l. During the last glacial period, certain species within Amaranthaceae s.l. underwent adaptations to different environments and began to differentiate rapidly. Since then, these species may have experienced morphological and genetic changes distinct from those of other genera due to intense selection pressure.

Hierarchical Composite with Self-Adaptive Anisotropic Deformation for Thermal Protection System.

Rigid thermal protection materials such as ultra-high-temperature ceramics are desirable for applications in aerospace vehicles, but few materials can currently satisfy the emerging high-temperature sealing requirements for dynamic gaps created by the mismatch of the thermal expansion of different protection layers. Here, we design and fabricate a flexible biomimetic anisotropic deformation composite by multilayer cocuring onto fiber fabrics. It displays superior anisotropic deformation, whose longitudinal expansion ratio is 48 times greater than the transverse expansion ratio at specific temperatures. Furthermore, the ordered carbon structure created by transition-metal-catalyzed graphitization and the C/Si synergistic effect resulting from the combination of biomimetic fiber fabrics and SR enable the in situ formation of a high-temperature-resistant SiC crystalline phase within the char layer, ultimately resulting in exceptional thermal protection properties. By constructing hollow structures in situ, the back temperature of the composite, which is only 4.33 mm thick, is stabilized at 140 °C under the condition of continuous butane flame ablation (1300 °C) for 420 s. Multilayer structure and flexible features can facilitate large-scale preparation and arbitrary cutting and bending, adapted to different thermal protection areas.

Innate immune and proinflammatory signals activate the Hippo pathway via a Tak1-STRIPAK-Tao axis.

The Hippo pathway controls developmental, homeostatic and regenerative tissue growth, and is frequently dysregulated in various diseases. Although this pathway can be activated by innate immune/inflammatory stimuli, the underlying mechanism is not fully understood. Here, we identify a conserved signaling cascade that leads to Hippo pathway activation by innate immune/inflammatory signals. We show that Tak1, a key kinase in innate immune/inflammatory signaling, activates the Hippo pathway by inducing the lysosomal degradation of Cka, an essential subunit of the STRIPAK PP2A complex that suppresses Hippo signaling. Suppression of STRIPAK results in the activation of Hippo pathway through Tao-Hpo signaling. We further show that Tak1-mediated Hippo signaling is involved in processes ranging from cell death to phagocytosis and innate immune memory. Our findings thus reveal a molecular connection between innate immune/inflammatory signaling and the evolutionally conserved Hippo pathway, thus contributing to our understanding of infectious, inflammatory and malignant diseases.