Microbial communities living in the same environment often display alternative stable states, each characterized by a unique composition of species. Understanding the origin and determinants of microbiome multistability has broad implications in environments, human health, and microbiome engineering. However, despite its conceptual importance, how multistability emerges in complex communities remains largely unknown. Here, we focused on the role of horizontal gene transfer (HGT), one important aspect mostly overlooked in previous studies, on the stability landscape of microbial populations. Combining mathematical modeling and numerical simulations, we demonstrate that, when mobile genetic elements (MGEs) only affect bacterial growth rates, increasing HGT rate in general promotes multistability of complex microbiota. We further extend our analysis to scenarios where HGT changes interspecies interactions, microbial communities are subjected to strong environmental selections and microbes live in metacommunities consisting of multiple local habitats. We also discuss the role of different mechanisms, including interspecies interaction strength, the growth rate effects of MGEs, MGE epistasis and microbial death rates in shaping the multistability of microbial communities undergoing HGT. These results reveal how different dynamic processes collectively shape community multistability and diversity. Our results provide key insights for the predictive control and engineering of complex microbiota.

Accurate regulation of centrosome size is essential for ensuring error-free cell division, and dysregulation of centrosome size has been linked to various pathologies, including developmental defects and cancer. While a universally accepted model for centrosome size regulation is lacking, prior theoretical and experimental works suggest a centrosome growth model involving autocatalytic assembly of the pericentriolar material. Here, we show that the autocatalytic assembly model fails to explain the attainment of equal centrosome sizes, which is crucial for error-free cell division. Incorporating latest experimental findings into the molecular mechanisms governing centrosome assembly, we introduce a new quantitative theory for centrosome growth involving catalytic assembly within a shared pool of enzymes. Our model successfully achieves robust size equality between maturing centrosome pairs, mirroring cooperative growth dynamics observed in experiments. To validate our theoretical predictions, we compare them with available experimental data and demonstrate the broad applicability of the catalytic growth model across different organisms, which exhibit distinct growth dynamics and size scaling characteristics.