KIZ located in one of the planet's most vibrant biological hotspots, here, groundbreaking research in primatology, evolutionary genetics, and biodiversity conservation isn't just theoretical. It's transforming how we understand health, sustain our planet, and innovate for the future.

Founded in April 1959, the Kunming Institute of Zoology, affiliated with the Chinese Academy of Sciences, is a comprehensive research institution in China focusing on biodiversity evolution, conservation, and sustainable utilization.

In a study published in Molecular Psychiatry on September 4, 2026, a team led by Xiao Xiao from the Kunming Institute of Zoology (KIZ) of the Chinese Academy of Sciences, along with collaborators from Jinan University and Xi'an Jiaotong University First Affiliated Hospital, integrated genome-wide association study data, whole-exome sequencing data, and human brain cortical developmental multi-omics data to identify cortical cell types underlying schizophrenia genetic risk. The researchers built an atlas of approximately 3 million nuclei from 325 neurotypical donors, using 22 public single-nucleus RNA sequencing datasets. The data spanned from early embryonic development to adulthood, covering the cingulate, frontal, motor, temporal, and visual cortices.

How domestication shapes brain evolution remains an open question. In this study, we integrated single-nucleus RNA sequencing (snRNA-seq), population genomics, and machine learning to investigate hippocampal evolution under domestication. Across-species comparisons revealed that hippocampal cell type profiles are largely conserved across vertebrate species, while supporting the presence of adult hippocampal neurogenesis in birds. We further found that domestication and selective breeding likely influence the cellular composition and molecular regulation of the hippocampus. Our findings provide cellular evidence supporting the hypothesis that domestication affects adult hippocampal neurogenesis. Additionally, we showed that genes associated with neural progenitor cells (NPCs) states and cell-marker programs are enriched for signatures of selection. Many of these genes function as regulators of neurogenesis and pathways mediating stress and fear reduction. Specifically, we identified selection at the FKBP5 promoter that may influence its expression in the NPC lineage, potentially contributing to stress-response regulation during domestication. Collectively, these results suggest that domestication is associated with hippocampal remodeling as part of an adaptive response to human-managed environments. This study provides a cellular and genetic perspective on how domestication reshapes the brain and offers a basis for further investigation into the mechanisms of neural evolution within the context of microevolution.

Embryonic stem cells (ESCs) exhibit a hyperactive chromatin state at ribosomal RNA (rRNA) genes, which not only plays roles in active rRNA synthesis and ribosome biogenesis (RiBi), but also links to genome architecture. However, how this active chromatin state is maintained in ESCs remains poorly understood. Here, we identify Tcf15, a mouse ESC-specific factor, as a novel regulator of ribosomal DNA (rDNA) chromatin state. Tcf15 localizes to the nucleolus, binds the coding region of rRNA genes, and independently recruits epigenetic modifiers—either Tet2 or Rbbp5 (a core component of H3K4 methyltransferases)—to promote an active chromatin configuration. Depletion of Tcf15 increases DNA methylation and H3K27me3 levels at rDNA. Intriguingly, the Tcf15-Rbbp5 axis ensures precursor rRNA transcription and RiBi, whereas the Tcf15-Tet2 axis is not involved in rRNA synthesis. Ribosome profiling further revealed compromised translation of a subset of mRNAs involved in DNA replication, damage response, and repair. Consequently, Tcf15- or Rbbp5-deficient ESCs exhibit severe genomic instability. Our findings add a new regulatory layer of chromatin state in rDNA of stem cells, and reveal a previously unrecognized phenotypic consequence of defective RiBi in ESCs.

Long-term culture of human embryonic stem cells (hESCs) often induces chromosomal abnormalities, which limits their clinical use. However, the underlying mechanisms are unclear. Early replication fragile sites (ERFSs) are genomic loci susceptible to breakage in early S-phase and serve as hotspots for chromosomal rearrangements, with established links to carcinogenesis. To map ERFSs in hESCs, we established the early S-phase synchronization protocols and identified ERFSs. These ERFSs are enriched in GC content and short interspersed nuclear elements (SINEs) and are frequently located in promoters or enhancers of genes involved in pluripotency, proliferation, and genomic stability. ERFSs also overlap with regions associated with copy number variants (CNVs) and single nucleotide variants (SNVs) linked to cancers. Furthermore, we found that chromatin accessibility contributes to ERFS formation. Collectively, these findings provide a key resource for advancing ERFS research, offering insights into the phenotypic and genomic alterations observed in long-term hESC cultures.

The complement system was originally discovered as a product of hepatocytes and immune cells secreted into circulation, mediating immune responses through the classical, lectin, and alternative pathways. However, recent findings have revealed that non-immune cells, including epithelial cells, endothelial cells, neurons, pancreatic islet cells, and fibroblasts, also express complement molecules localized to organelles such as lysosomes, endoplasmic reticulum, and mitochondria, forming an intracellular complement system independent of circulating complement. Named the "complosome," this system regulates apoptosis, metabolism, autophagy, and gene expression.

Myelin sheaths wrap neuronal axons and are essential for rapid nerve impulse conduction. Their formation depends on the proliferation, differentiation, and maturation of oligodendrocyte precursor cells (OPCs). Because myelination involves massive membrane expansion and high metabolic activity, OPCs face persistent oxidative stress. In a study published in Advanced Science, a team led by Prof. Mao Bingyu from the Kunming Institute of Zoology (KIZ), in collaboration with Prof. Zhao Shuhua's team at the First Affiliated Hospital of Kunming Medical University, revealed that the E3 ubiquitin ligase RLIM safeguards oligodendrocyte development and myelination by targeting SLC7A11 for polyubiquitination to regulate ferroptotic resistance.

Pigs are not only important agricultural animals but also key model organisms for studying evolution, complex traits, and human diseases. As genome sequencing and genetic research advance, numerous genetic variants associated with pig domestication, economic traits, and disease have been identified. However, many key variants reside in non-coding regions, and traditional linear genome annotation cannot determine which genes these regulatory variants act upon. In a study published in Molecular Biology and Evolution on July 30, 2026, a team led by Prof. Zhang Yaping from the Kunming Institute of Zoology (KIZ), along with collaborators from the University of Science and Technology of China and Yunnan University, constructed Pig Matrix, a multi-omics 3D regulatory genomics database for pigs.

The "Frontiers in Asian Herpetology" forum was held in Kunming, Yunnan, on 21–23 June 2026. Co‑hosted by KIZ and partner institutions, it brought together over 50 researchers from China and seven other countries. Scientific sessions covered evolution, biogeography, conservation genomics, and behavioural adaptation. The forum fostered international exchange and laid a foundation for cross‑disciplinary collaboration in Asian herpetology.