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Moso‐bamboo (Phyllostachys edulis), with the favor of human disturbance, rapidly invades adjacent forests to form monocultures in East Asia. Moso‐bamboo not only intrudes the broadleaf forests but also the coniferous, and it could impact by above‐ and below‐ground pathways. However, it still remains unclear whether the below‐ground performance of moso‐bamboo differs from broadleaf to coniferous forests, especially those differing in competitive and nutrient acquisition strategies. In this study, we investigated three types of forest stands in Guangdong, China, including a bamboo monoculture, a coniferous forest, and a broadleaf forest. We found that moso‐bamboo may suffer stronger soil P limitation (soil N/P = 18.16) and may be infected by more AMF in coniferous than broadleaf forests (soil N/P = 16.17). Based on our PLS‐path model analysis, soil P resource may be the key to differ moso‐bamboo root morphology and rhizosphere microbe in different forests: in broadleaf forests with weaker soil P limitation, may be realized through increasing specific root length and specific surface area, whereas in coniferous forests with stronger soil, P limitation may be realized through combining more AMF. Our study highlights the importance of underground mechanisms about moso‐bamboo expansion in different forest communities. [ABSTRACT FROM AUTHOR]

Metastasis associated lung adenocarcinoma transcript 1( MALAT1) is a long non-coding RNA, broadly expressed in mammalian tissues including kidney and up-regulated in a variety of cancer cells. To date, its functions in podocytes are largely unknown. β-catenin is a key mediator in the canonical and non-canonical Wnt signalling pathway; its aberrant expression promotes podocyte malfunction and albuminuria, and contributes to kidney fibrosis. In this study, we found that MALAT1 levels were increased in kidney cortices from C57 BL/6 mice with streptozocin ( STZ)-induced diabetic nephropathy, and dynamically regulated in cultured mouse podocytes stimulated with high glucose, which showed a trend from rise to decline. The decline of MALAT1 levels was accompanied with β-catenin translocation to the nuclei and enhanced expression of serine/arginine splicing factor 1 ( SRSF1), a MALAT1 RNA-binding protein. Further we showed early interference with MALAT1 si RNA partially restored podocytes function and prohibited β-catenin nuclear accumulation and SRSF1 overexpression. Intriguingly, we showed that β-catenin was involved in MALAT1 transcription by binding to the promotor region of MALAT1; β-catenin knock-down also decreased MALAT1 levels, suggesting a novel feedback regulation between MALAT1 and β-catenin. Notably, β-catenin deletion had limited effects on SRSF1 expression, demonstrating β-catenin might serve as a downstream signal of SRSF1. These findings provided evidence for a pivotal role of MALAT1 in diabetic nephropathy and high glucose-induced podocyte damage. [ABSTRACT FROM AUTHOR]

Fyn, a member of the Src family of tyrosine kinases, is a key regulator in cytoskeletal remodeling in a variety of cell types. Recent studies have demonstrated that Fyn is responsible for nephrin tyrosine phosphorylation, which will result in polymerization of actin filaments and podocyte damage. Thus detailed involvement of Fyn in podocytes is to be elucidated. In this study, we investigated the potential role of Fyn/ROCK signaling and its interactions with paxillin. Our results presented that high glucose led to filamentous actin (F-actin) rearrangement in podocytes, accompanied by paxillin phosphorylation and increased cell motility, during which Fyn and ROCK were markedly activated. Gene knockdown of Fyn by siRNA showed a reversal effect on high glucose-induced podocyte damage and ROCK activation; however, inhibition of ROCK had no significant effects on Fyn phosphorylation. These observations demonstrate that in vitro Fyn mediates high glucose-induced actin cytoskeleton remodeling of podocytes via promoting ROCK activation and paxillin phosphorylation. [ABSTRACT FROM AUTHOR]

"Dao", as a basic concept of Chinese philosophy has been widely used in Chinese aesthetics, and has also been a basic terminology and logical starting point of various kinds of art description and explanation. In aesthetics, "Dao" has three major significances, namely, the foundation of the existence of art, the creation law of art, and the aesthetic realm of art. Therefore, the art itself is accordingly regarded as the revealing of "Dao". [ABSTRACT FROM AUTHOR]

Intellectual disability (ID) affects ~2% of the population and ID-associated genes are enriched for epigenetic factors, including those encoding the largest family of histone lysine acetyltransferases (KAT5-KAT8). Among them is KAT6A , whose mutations cause KAT6A syndrome, with ID as a common clinical feature. However, the underlying molecular mechanism remains unknown. Here, we find that KAT6A deficiency impairs synaptic structure and plasticity in hippocampal CA3, but not in CA1 region, resulting in memory deficits in mice. We further identify a CA3-enriched gene Rspo2 , encoding Wnt activator R-spondin 2, as a key transcriptional target of KAT6A. Deletion of Rspo2 in excitatory neurons impairs memory formation, and restoring RSPO2 expression in CA3 neurons rescues the deficits in Wnt signaling and learning-associated behaviors in Kat6a mutant mice. Collectively, our results demonstrate that KAT6A-RSPO2-Wnt signaling plays a critical role in regulating hippocampal CA3 synaptic plasticity and cognitive function, providing potential therapeutic targets for KAT6A syndrome and related neurodevelopmental diseases.