Golshani, S. | Search bioRxiv

bioRxiv2026

Belowground functional traits predict population temporal stability in grasslands

Temporal stability of plant populations is a key determinant of species coexistence and ecosystem functioning, yet its trait-based explanation has remained largely aboveground. Whether root functional traits contribute to long-term population stability remains poorly understood, despite roots mediating water and nutrient acquisition. We combined 17 years of vegetation monitoring from 150 temperate grassland plots across three regions in Germany with root functional trait data for 72 common grassland species. Temporal stability was computed as coefficient of variation (CV), with lower CV indicating higher stability. We tested whether root traits predict stability, and specifically which belowground dimensions from resource acquisition/conservation or soil exploration dominate, and whether differences in land use intensity modifies these relationships. Root traits were stronger and more consistent predictors of temporal stability than the classical aboveground traits specific leaf area (SLA) and leaf dry matter content (LDMC). Higher average root diameter (AD), root hair incidence (RHI), specific root length (SRL), and root tissue density (RTD) were generally associated with higher temporal stability, although the strength of these relationships varied among regions. Land use modified selected trait and stability relationships, with the strongest shifts occurring along the mowing gradient. Increasing mowing strengthened the associations of higher RHI and RTD with temporal stability, whereas the associations of AD and root N shifted towards lower stability. Our results identify belowground functional traits as an important missing component of trait-based temporal stability research and advance our understanding of the functional strategies underlying population temporal stability in managed semi-natural grasslands.

ecology↗

bioRxiv2023

Modulation of cannabinoid receptor 2 alters neuroinflammation and reduces formation of alpha-synuclein aggregates in a rat model of nigral synucleinopathy

Research into the disequilibrium of microglial phenotypes has become an area of intense focus in neurodegenerative disease as a potential mechanism that contributes to chronic neuroinflammation and neuronal loss in Parkinsons disease (PD). There is growing evidence that neuroinflammation accompanies and may promote progression of alpha-synuclein (Asyn)-induced nigral dopaminergic (DA) degeneration. From a therapeutic perspective, development of immunomodulatory strategies that dampen overproduction of pro-inflammatory cytokines from chronically activated immune cells and induce a pro-phagocytic phenotype is expected to promote Asyn removal and protect vulnerable neurons. Cannabinoid receptor-2 (CB2) is highly expressed on activated microglia and peripheral immune cells, is upregulated in the substantia nigra of individuals with PD and in mouse models of nigral degeneration. Furthermore, modulation of CB2 protects against rotenone-induced nigral degeneration; however, CB2 has not been pharmacologically and selectively targeted in an Asyn model of PD. Here, we report that 7 weeks of peripheral administration of CB2 inverse agonist SMM-189 reduced phosphorylated (pSer129) alpha-synuclein in the substantia nigra compared to vehicle treatment. Additionally, SMM-189 delayed Asyn-induced immune cell infiltration into the brain as determined by flow cytometry, increased CD68 protein expression, and elevated wound-healing-immune-mediator gene expression. Additionally, peripheral immune cells increased wound-healing non-classical monocytes and decreased pro-inflammatory classical monocytes. In vitro analysis of RAW264.7 macrophages treated with lipopolysaccharide (LPS) and SMM-189 revealed increased phagocytosis as measured by the uptake of fluorescence of pHrodo E. coli bioparticles. Together, results suggest that targeting CB2 with SMM-189 skews immune cell function toward a phagocytic phenotype and reduces toxic aggregated species of Asyn. Our novel findings demonstrate that CB2 may be a target to modulate inflammatory and immune responses in proteinopathies.

immunology↗