Biology subjects

Kim, J.-Y.

Publications and source records attributed to Kim, J.-Y..

4 recordsLinked to original sources

bioRxiv2018

Altitudinal range-size distribution of breeding birds and environmental factors for the determination of species richness: An empirical test of altitudinal Rapoports rule and rescue effect on a local scale

Range-size distributions are important for understanding species richness patterns and led to the development of the controversial Rapoports rule and Rapoport-rescue effect. This study aimed to understand the relationship between species richness and range-size distribution in relation to environmental factors. The present study tested the following: (1) altitudinal Rapoports rule, (2) climatic and ambient energy hypotheses, (3) non-directional rescue effect, and (4) effect of environmental factors on range-size group. Altitudinal species range-size distribution increased with increasing altitude and showed a negative relationship with climatic variables and habitat heterogeneity, and a positive relationship with primary productivity. These results support the altitudinal Rapoports rule and climatic hypothesis; however, they do not fully support the ambient energy hypothesis. Results from testing the non-directional rescue effect showed that the inflow intensity of species from both directions (high and low elevations) affected species richness. And we found that the 2nd and 3rd quartile species distribution were the main cause of a mid-peak of species richness and the non-directional rescue effect. Additionally, the 2nd quartile species richness was highly related to minimum temperature and possessed thermal specialist species features, and the 3rd quartile species richness was highly related to habitat heterogeneity and primary productivity. Although altitudinal range-size distribution results were similar to the altitudinal Rapoports rule, the mid-peak pattern of species richness could not be explained by the Rapoports-rescue effect; however, the non-directional rescue effect could explain a mid-peak pattern of species richness.

ecology↗

bioRxiv2018

Depleting Trim28 in adult mice is well tolerated and reduces levels of α-synuclein and tau

Alzheimers and Parkinsons disease are late onset neurodegenerative diseases that will require therapy over decades to mitigate the effects of disease-driving proteins such tau and -synuclein (-Syn). We recently found that TRIM28 regulates the levels and toxicity of -Syn and tau (Rousseaux et al., 2016), however, how TRIM28 regulates -Syn and whether its chronic inhibition later in life is safe remained unknown. Here, we show that TRIM28 mediates the SUMOylation of -Syn and tau, and that genetic suppression of Trim28 in adult mice is compatible with life. We were surprised to see that mice lacking Trim28 in adulthood do not exhibit behavioral or pathological phenotypes, and importantly, adult reduction of TRIM28 results in a decrease of -Syn and tau levels. These results suggest that deleterious effects from TRIM28 depletion are limited to development and that its inhibition adulthood provides a potential path for modulating -Syn and tau levels.

neuroscience↗

bioRxiv2017

KDM2B is a histone H3K79 demethylase and induces transcriptional repression via SIRT1-mediated chromatin silencing

The methylation of histone H3 lysine 79 (H3K79) is an active chromatin marker and is prominant in actively transcribed regions of the genome. However, demethylase of H3K79 remains unknown despite intensive research. Here, we show that KDM2B (also known as FBXL10), a member of the Jumonji C family of proteins and known for its histone H3K36 demethylase activity, is a di- and tri-methyl H3K79 demethylase. We demonstrate that KDM2B induces transcriptional repression of HOXA7 and MEIS1 via occupancy of promoters and demethylation of H3K79. Furthermore, genome-wide analysis suggests that H3K79 methylation levels increase when KDM2B is depleted, indicating that KDM2B functions as an H3K79 demethylase in vivo. Finally, stable KDM2B-knockdown cell lines exhibit displacement of NAD+-dependent deacetylase SIRT1 from chromatin, with concomitant increases in H3K79 methylation and H4K16 acetylation. Our findings identify KDM2B as an H3K79 demethylase and link its function to transcriptional repression via SIRT1-mediated chromatin silencing.

genetics↗

bioRxiv2017

Comparative transcriptome profiling of the human and mouse dorsal root ganglia: An RNA-seq-based resource for pain and sensory neuroscience research

Molecular neurobiological insight into human nervous tissues is needed to generate next generation therapeutics for neurological disorders like chronic pain. We obtained human Dorsal Root Ganglia (DRG) samples from organ donors and performed RNA-sequencing (RNA-seq) to study the human DRG (hDRG) transcriptional landscape, systematically comparing it with publicly available data from a variety of human and orthologous mouse tissues, including mouse DRG (mDRG). We characterized the hDRG transcriptional profile in terms of tissue-restricted gene co-expression patterns and putative transcriptional regulators, and formulated an information-theoretic framework to quantify DRG enrichment. Our analyses reveal an hDRG-enriched protein-coding gene set (~140), some of which have not been described in the context of DRG or pain signaling. A majority of these show conserved enrichment in mDRG, and were mined for known drug - gene product interactions. Comparison of hDRG and tibial nerve transcriptomes suggest pervasive mRNA transport of sensory neuronal genes to axons in adult hDRG, with potential implications for mechanistic insight into chronic pain in patients. Relevant gene families and pathways were also analyzed, including transcription factors (TFs), g-protein coupled receptors (GCPRs) and ion channels. We present our work as an online, searchable repository (http://www.utdallas.edu/bbs/painneurosciencelab/DRGtranscriptome), creating a valuable resource for the community. Our analyses provide insight into DRG biology for guiding development of novel therapeutics, and a blueprint for cross-species transcriptomic analyses.\n\nSummaryWe generated RNA sequencing data from human DRG samples and comprehensively compared this transcriptome to other human tissues and a matching panel of mouse tissues. Our analysis uncovered functionally enriched genes in the human and mouse DRG with important implications for understanding sensory biology and pain drug discovery.

neuroscience↗