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Nature Ecology & Evolution · 2024 ·Vol. 8 ·期 3 ·392-399 · IF 13.9

Microbe-induced phenotypic variation leads to overyielding in clonal plant populations

Raza Waseem,Jiang Gaofei,Eisenhauer Nico,Huang Yishuo,Wei Zhong,Shen Qirong,Kowalchuk George A.,Jousset Alexandre

Overyielding, the high productivity of multispecies plant communities, is commonly seen as the result of plant genetic diversity. Here we demonstrate that biodiversity–ecosystem functioning relationships can emerge in clonal plant populations through interaction with microorganisms. Using a model clonal plant species, we found that exposure to volatiles of certain microorganisms led to divergent plant phenotypes. Assembling communities out of plants associated with different microorganisms led to transgressive overyielding in both biomass and seed yield. Our results highlight the importance of belowground microbial diversity in plant biodiversity research and open new avenues for precision ecosystem management.

研究领域: 植物学 · 生态学 · 微生物学

✓ 已验证 DOI PubMed 高影响因子

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BLOOD · 2025 ·Vol. 145 ·期 10 ·1074-1088 · IF 23.1

Mutations in AMBRA1 aggravate β-thalassemia by impairing autophagy-mediated clearance of free α-globin

Yong Long,Qianqian Zhang,Ling Ling,Yuan Zhuang,Xiaolei Wei,Haoyang Huang,Zhanping Lu,Yushan Huang,Xianming Chen,Yuhua Ye,Xiaoqin Feng,Haokun Zhang,Binbin Huang,Yueyan Huang,Yidan Liang,Mingyan Fang,Yukio Nakamura,Bin Lin,Xinhua Zhang,Daru Lu,Xin Jin,Xiangmin Xu

Accumulation of free α-globin is a critical factor in the pathogenesis of β-thalassemia. Autophagy plays a crucial role in clearing toxic free α-globin, thereby reducing disease severity. However, the impact of natural mutations in autophagy-related genes (ATGs) on the phenotypic variability of β-thalassemia remains unclear. In this study, we systematically investigated the relationship between variants in ATGs and disease phenotypes in a cohort of 1022 patients with β-thalassemia, identifying 4 missense mutations in the autophagy and beclin 1 regulator 1 (AMBRA1) gene. Disruption of the Ambra1 gene in β-thalassemic mice was found to reduce autophagic clearance of α-globin in red blood cell precursors, exacerbating disease phenotypes. Functional characterization of the AMBRA1 gene and these mutations in patient-derived CD34+ cells, edited human umbilical cord blood–derived erythroid progenitor 2 (HUDEP-2) cells, and engineered HUDEP-2 β-thalassemic cells confirmed that AMBRA1 facilitates the autophagic clearance of free α-globin in human erythroid cells. Functional studies demonstrated that AMBRA1 missense mutants destabilize Unc-51-like kinase 1 protein, inhibit light chain 3 protein lipidation, and subsequently hinder autophagic flux, leading to increased α-globin deposition. Additionally, these mutations were associated with erythrotoxic effects in vitro, including increased intracellular reactive oxygen species levels, higher apoptosis rates, and impaired erythroid differentiation and maturation. This study sheds light on the molecular association between mutations in ATGs and the exacerbation of β-thalassemia, highlighting the potential role of the AMBRA1 gene as a promising diagnostic and therapeutic target for β-hemoglobinopathies.

CAS / MDL: 50-02-2

研究领域: 血液学 · 分子生物学 · 遗传学

✓ 已验证产品关联 DOI PubMed 高影响因子

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Microbe-induced phenotypic variation leads to overyielding in clonal plant populations

Mutations in AMBRA1 aggravate β-thalassemia by impairing autophagy-mediated clearance of free α-globin