Wang, Y. Z. | Search bioRxiv

bioRxiv2025

Proteomic analysis reveals distinct germination strategies in polymorphic fruits of Haloxylon ammodendron

Fruit polymorphism, the production of multiple fruit morphotypes within a species, is an adaptive bet-hedging strategy in variable environments. However, researches about perennial plant and the adaptive mechanisms are not well understood. Haloxylon ammodendron, a constructive desert shrub, exhibits three fruit morphotypes: YY (yellow wings with yellow pericarp), YP (yellow wings with pink pericarp), and PP (pink wings with pink pericarp). We investigated their ecophysiological and molecular mechanisms through germination assays under salt and drought stress, combined with proteomic analysis. YP consistently showed the highest germination percentage (GP) and germination rate index (GRI) under stress, while PP displayed well germination success under low salinity and well-watered conditions (GP=32.7%, 36.7%; GRI=0.018, 0.020), but significantly impaired viability under stress (GP=12.7%, 12.0%; GRI=0.006, 0.006). Proteomics identified 721 differentially expressed proteins (DEPs), with the most (662) between YP and PP, linked to stress response and germination. YPs high abundance of stress-resistant proteins enabled rapid germination, whereas PPs delayed germination aligns with a persistent seed bank strategy. This polymorphism promotes niche differentiation: YP ensures quick colonization, PP enhances long-term resilience, and YY offers an intermediate strategy. Our findings reveal molecular-ecological adaptations in H. ammodendron, aiding targeted germplasm use for desert restoration.

plant biology↗

bioRxiv2022

Rescue of neuropsychiatric phenotypes in a mouse model of 16p11.2 duplication syndrome by genetic correction of an epilepsy network hub

Neuropsychiatric disorders (NPDs) share genetic etiology and are frequently co-morbid with epilepsy, but the biological basis of this shared risk remains poorly understood. The 16p11.2 microduplication (16p11.2dup/+) is a highly pleiotropic copy number variant (CNV) conferring risk for multiple NPDs including autism spectrum disorder, schizophrenia and intellectual disability, and is associated with a high prevalence of seizures. We used a mouse model of the 16p11.2 duplication (16p11.2dup/+) to uncover molecular and circuit properties associated with this broad phenotypic spectrum, and examined genes within the locus capable of phenotype reversal. Quantitative proteomics of cortical membranes revealed alterations to synaptic protein networks and products of diverse NPD risk genes in 16p11.2dup/+ mice. Network analysis identified an epilepsy-associated protein subnetwork, which was dysregulated in 16p11.2dup/+ mice and proteomic datasets from human NPDs. We investigated circuit properties in 16p11.2dup/+ mice and found they exhibited hypersynchronous activity and enhanced network glutamate release, which increased susceptibility to seizures. We hypothesized that a regulator of the synaptic and epilepsy-associated protein network could have an important impact on pathophysiology. Human brain co-expression and interactome analysis revealed PRRT2 as a major hub in the dysregulated epilepsy subnetwork. Remarkably, restoring Prrt2 copy number to wild-type levels rescued aberrant circuit properties, seizure susceptibility and social interaction deficits in 16p11.2dup/+ mice. We show that proteomics and network biology can identify important disease hubs in multigenic CNVs, and reveal molecular and circuit phenotypes which may be relevant to the complex symptomatology of 16p11.2 duplication carriers.

neuroscience↗