DING, B. | bioRxiv Science

bioRxiv2026

Ancient tandem duplication of CYCLOIDEA is associated with the evolution of capitulum development in Asteraceae

Asteraceae is one of the largest and most diverse families of flowering plants. Much of their evolutionary success is attributed to their unique inflorescence structure-the capitulum. Despite their profound adaptive and taxonomic significance, the evolutionary genetic mechanisms underlying Asteraceae capitulum diversification remains poorly understood. We integrated comparative genomic analyses of 35 Asteraceae genomes with developmental transcriptome profiling of ray and disc florets. Our results uncovered a deeply conserved CYC2e-CYC2c-CYC2d-CYC2g-CYC2b tandem gene cluster that is prevalent across the Asteraceae family. We demonstrated that this tandem cluster arose during the early evolutionary diversification of Asteraceae. Subsequent lineage-specific gene retention and loss events have reshaped the composition of this cluster across different Asteraceae lineages. Notably, key members of this cluster, particularly CYC2c, CYC2d, and CYC2g, are preferentially retained in lineages with ray florets, which is consistent with their roles in regulating the ray floret development. Collectively, our findings establish a mechanistic link between the evolutionary divergence, spatiotemporal expression differentiation of the CYC2 tandem cluster as a key genetic driver underlying the morphological diversification and evolutionary success of Asteraceae.

evolutionary biology↗

bioRxiv2020

Disease modeling with human neurons reveals LMNB1 dysregulation underlying DYT1 dystonia

DYT1 dystonia is a hereditary neurological disease caused by a heterozygous mutation in torsin A (TOR1A). While animal models provide insights into disease mechanisms, significant species-dependent differences exist since mice with the identical heterozygous mutation fail to show pathology. Here, we model DYT1 by using human patient-derived motor neurons. These neurons with the heterozygous TOR1A mutation show markedly thickened nuclear lamina, disrupted nuclear morphology, and impaired nucleocytoplasmic transport, whereas they lack the perinuclear "blebs" that are often observed in animal models. Importantly, we further uncover that the nuclear lamina protein LMNB1 is specifically dysregulated in expression and subcellular localization. LMNB1 downregulation can largely ameliorate all the cellular defects in DYT1 motor neurons. These results reveal the value of disease modeling with human neurons and provide novel molecular mechanisms underlying DYT1 dystonia and potentially other neurological diseases with impaired nucleocytoplasmic transport.

neuroscience↗