Nakatani, A. | bioRxiv Science

bioRxiv2025

Fertilization reduces aphid performance but does not alter competitive exclusion between specialist and generalist species

Understanding how resource availability shapes herbivore competitive interactions is crucial for predicting pest dynamics under changing agricultural practices. Interspecific competition among herbivorous insects is mediated by host plant quality, yet mechanisms underlying competitive outcomes under varying nutrient conditions remain unclear. We investigated how fertilization affects population dynamics and competitive interactions between the legume-specialist Megoura crassicauda and the generalist Aphis craccivora on pea shoots (Pisum sativum) under fertilized and unfertilized conditions. Aphid population dynamics were monitored for 30 days in single-species and mixed-species treatments, and plant survival and biomass changes were assessed. Unexpectedly, fertilization reduced aphid population growth in both species, challenging conventional assumptions about nutrient effects on herbivores. Fertilization significantly affected M. crassicauda population growth but not that of A. craccivora. In mixed treatments, A. craccivora consistently excluded M. crassicauda by day 25, regardless of nutrient status. Plant mortality occurred in all aphid treatments except M. crassicauda under fertilized conditions. Our findings demonstrate that nutrient enrichment reduced herbivore performance but did not alleviate interspecific competition. The consistent competitive dominance of the generalist suggests that intrinsic species traits, rather than resource availability, determine competitive hierarchies. These findings have implications for pest management under changing agricultural practices.

ecology↗

bioRxiv2020

Inhibition of KDM1A activity restores adult neurogenesis and improves hippocampal memory in a mouse model of Kabuki syndrome

Kabuki syndrome (KS) is a rare cause of intellectual disability primarily caused by loss of function mutations in lysine-specific methyltransferase 2D (KMT2D), which normally adds methyl marks to lysine 4 on histone 3. Previous studies have shown that a mouse model of KS (Kmt2d+/{beta}Geo) demonstrates disruption of adult neurogenesis and hippocampal memory. Proof-of-principle studies have shown postnatal rescue of neurological dysfunction following treatments that promote chromatin opening, however, these strategies are non-specific and do not directly address the primary defect of histone methylation. Since lysine-specific demethylase 1A (LSD1/KDM1A) normally removes the H3K4 methyl marks added by KMT2D, we hypothesize that inhibition of KDM1A demethylase activity may ameliorate molecular and phenotypic defects stemming from KMT2D loss. To test this hypothesis, we evaluated a recently developed KDM1A inhibitor (TAK-418) in Kmt2d+/{beta}Geo mice. We find that orally administered TAK-418 increases the numbers of newly born Doublecortin (DCX)+ cells and processes in hippocampus in a dose dependent manner. We also observe TAK-418-dependent rescue of histone modification defects in hippocampus both by Western blot and ChIP-Seq. Treatment rescues gene expression abnormalities including those of immediate early genes such as FBJ osteosarcoma oncogene (Fos) and FBJ osteosarcoma oncogene homolog B (Fosb). After 2 weeks of TAK-418, Kmt2d+/{beta}Geo mice demonstrate normalization of hippocampal memory defects. In summary, our data suggest that KDM1A inhibition is a plausible treatment strategy for KS and support the hypothesis that the epigenetic dysregulation secondary to KMT2D dysfunction plays a major role in the postnatal neurological disease phenotype in KS.

genetics↗