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Simple Summary: Bamboo part preference and a panda's age have been shown to shift the gut microbiota composition of the giant panda, thus eliciting changes in their nutrient utilization capacity. The present study compared the differences in nutrient digestibility and fecal microbiota composition between adult and geriatric captive giant pandas when fed exclusively with a diet comprising of either bamboo shoots or leaves. Bamboo part preference exerted a significant effect on nutrient digestibility and fecal microbiota composition in both adult and aged giant pandas. Bamboo part dominated over age in shaping the nutrient digestibility and gut microbiota composition of giant pandas. Bamboo part preference plays a critical role in influencing the nutrient utilization and gastrointestinal microbiota composition of captive giant pandas. However, the effects of bamboo part consumption on the nutrient digestibility and gut microbiome of geriatric giant pandas remain unknown. A total of 11 adult and 11 aged captive giant pandas were provided with bamboo shoots or bamboo leaves in the respective single-bamboo-part consumption period, and the nutrient digestibility and fecal microbiota of both adult and aged giant pandas in each period were evaluated. Bamboo shoot ingestion increased the crude protein digestibility and decreased the crude fiber digestibility of both age groups. The fecal microbiome of the bamboo shoot-fed giant pandas exhibited greater alpha diversity indices and significantly different beta diversity index than the bamboo leaf-fed counterparts regardless of age. Bamboo shoot feeding significantly changed the relative abundance of predominant taxa at both phylum and genus levels in adult and geriatric giant pandas. Bamboo shoot-enriched genera were positively correlated with crude protein digestibility and negatively correlated with crude fiber digestibility. Taken together, these results suggest that bamboo part consumption dominates over age in affecting the nutrient digestibility and gut microbiota composition of giant pandas. [ABSTRACT FROM AUTHOR]

Chloroplast-to-nucleus retrograde signaling is essential for the coupled expression of photosynthesis-associated nuclear genes (PhANGs) and plastid genes (PhAPGs) to ensure the functional status of chloroplasts (Cp) in plants. Although various signaling components involved in the process have been identified in Arabidopsis (Arabidopsis thaliana), the biological relevance of such coordination remains an enigma. Here, we show that the uncoupled expression of PhANGs and PhAPGs contributes to the cell death in the lesion simulating disease1 (lsd1) mutant of Arabidopsis. A daylength-dependent increase of salicylic acid (SA) appears to rapidly up-regulate a gene encoding SIGMA FACTOR BINDING PROTEIN1 (SIB1), a transcriptional coregulator, in lsd1 before the onset of cell death. The dual targeting of SIB1 to the nucleus and the Cps leads to a simultaneous up-regulation of PhANGs and down-regulation of PhAPGs. Consequently, this disrupts the stoichiometry of photosynthetic proteins, especially in PSII, resulting in the generation of the highly reactive species singlet oxygen (1O2) in Cps. Accordingly, inactivation of the nuclear-encoded Cp protein EXECUTER1, a putative 1O2 sensor, significantly attenuates the lsd1 -conferred cell death. Together, these results provide a pathway from the SA- to the 1O2-signaling pathway, which are intertwined via the uncoupled expression of PhANGs and PhAPGs, contributing to the lesion-mimicking cell death in lsd1. [ABSTRACT FROM AUTHOR]

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death worldwide. Homeobox D9 (HOXD9), a member of the HOX family of transcription factors, plays a driver role in development of multiple cancers. Angiopoietin-2 (ANGPT2) is reportedly to facilitate angiogenesis, growth and metastasis in various cancers, including lung cancer. In addition, blocking ANGPT2 can effectively improve cancer immunotherapy via downregulation of Programmed death ligand-1 (PD-L1). The purpose of this study was to elucidate the role of HOXD9 in NSCLC and whether ANGPT2 is required for HOXD9-mediated malignant behaviors of NSCLC cells. By performing a series of in vitro functional experiments, we found that knockdown of HOXD9 induced proliferative inhibition, cell cycle G1 arrest, apoptosis, migratory suppression and invasive repression of NSCLC cells. Reduced PD-L1 expression in NSCLC cells was observed after HOXD9 silencing. Besides, HOXD9 deletion decreased the expression of ANGPT2 in NSCLC cells. In line with this, HOXD9 overexpression led to opposite alteration in NSCLC cells. Mechanistically, ANGPT2 was transcriptionally activated by HOXD9. Forced expression of ANGPT2 significantly regulated HOXD9-mediated malignant phenotypes, and enhanced PD-L1 expression of NSCLC cells. Our results expressing HOXD9 may function as an oncogene in NSCLC via trans-activation of ANGPT2. [ABSTRACT FROM AUTHOR]