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Ngo, K. M.

Publications and source records attributed to Ngo, K. M..

2 recordsLinked to original sources

Stabilising selection and ecological trade-offs underpin coexistence in a tropical flora

Tropical forests harbour the majority of global plant biodiversity1,2, yet the genomic mechanisms governing the assembly and maintenance of these communities remain poorly understood. Here, we assembled draft genomes for 499 angiosperm species from a lowland rainforest in Singapore, representing 67% of its flora, and integrated these with plant traits and comprehensive forest census data. Across the community, most gene families evolve under stabilising selection, with copy numbers maintained near long-term optima that differ among ecological strategies. These niche-associated genomic attractor states provide a mechanism for convergent adaptation and species coexistence. Modelling stabilising selection also identified a strong trade-off between defence and growth, indicating that pathogen pressure constrains developmental diversification. Consistent with this, species-specific genome space was enriched for resistance genes and transposable elements. In contrast, genomic processes structuring present-day plant community composition differ from those driving deep-time convergence. Genomic comparisons across forest types revealed stronger selection on defence-related pathways in old-growth primary forests and on growth-related processes in regenerating secondary forests, while community-level genomic profiles showed expansions in gene families associated with rapid responses to environmental fluctuations. Stabilising selection therefore links population-level adaptation3,4 with long-term species diversification in the tropics. Niche similarity promotes long-term coexistence, whereas local community structure is shaped by more rapid ecological filtering driven by environmental change. Taken together, these two distinct evolutionary layers provide a genomic framework for understanding how hyperdiverse rainforest floras arise and persist.

genomics↗

SMAD6 Integrates Endothelial Cell Homeostatic Flow Responses Downstream of Notch

ABSTRACTLaminar shear stress regulates blood vessel morphogenesis and subsequent quiescence, leading to vascular homeostasis. Although important for vessel function, how vascular homeostasis is set up and maintained is poorly understood. SMAD6, a scaffold for several signaling pathways, is expressed in developing arteries and its expression is flow-regulated. We found that SMAD6 is essential for endothelial cell flow-mediated responses downstream of the mechanosensor Notch1. Endothelial cells with reduced SMAD6 levels failed to align under homeostatic laminar shear flow, while forced SMAD6 expression rescued misalignment induced by reduced Notch1 signaling. SMAD6-dependent homeostatic laminar flow responses required the Notch ligand Dll4 and Notch transcriptional activity. Mechanistically, neither the N-terminal nor the C-terminal domain of SMAD6 alone rescued flow alignment upon loss of Notch signaling. Endothelial cells with reduced Smad6 levels had compromised barrier function, and RNA profiling revealed upregulation of proliferation-associated genes and down regulation of junction-associated genes. Among junction-related genes affected by SMAD6 levels, the proto-cadherin PCDH12 was upregulated by homeostatic flow and required for proper flow-mediated endothelial cell alignment. Thus, SMAD6 is a critical integrator of flow-mediated signaling inputs downstream of Notch1, as vessels transition from an angiogenic to a homeostatic phenotype.Competing Interest StatementThe authors have declared no competing interest.View Full Text

cell biology↗