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Biology subjects

Kim, W. T.

Publications and source records attributed to Kim, W. T..

2 recordsLinked to original sources

The STA1-DOT2 interaction promotes nuclear speckle formation and splicing robustness in growth and heat stress responses

Pre-mRNA splicing is carried out by the spliceosome, a large and dynamic ribonucleoprotein complex. The spliceosome is known to be stored in nuclear speckles (NS), which are now recognized as active subnuclear organelles for splicing. However, it remains poorly understood how spliceosomal protein-protein interactions are functionally coupled to NS organization to maintain splicing robustness in plants. Here, we report the functional significance of a specific interaction between two U4/U6{middle dot}U5 tri-snRNP components of the spliceosome, STA1 and DOT2, in regulating NS organization, pre-mRNA splicing, and heat stress responses in Arabidopsis. We identified a missense mutation in DOT2 (a Snu66/SART1 homolog) from a genetic suppressor of the PRP6 homolog mutant sta1-1 (named S307). This mutation restored the weakened interaction between STA1 and DOT2 in the sta1-1 mutant background. Genetic, biochemical, and cell biological analyses showed that variation in the strength of the STA1-DOT2 interaction was closely associated with changes in NS formation, splicing efficiency, as well as growth and heat tolerance. Pharmacological inhibition of STA1-associated NS formation by tubercidin recapitulated sta1-1-like phenotypes and splicing defects, supporting a functional link between NS organization and splicing outcomes. In addition, heat-induced weakening of the STA1-DOT2 interaction was accompanied by reduced NS formation and increased intron retention at the transcriptome-wide level including key heat-responsive transcripts. Based on these observations, we propose that the STA1-DOT2 interaction, likely reflecting the assembly state of the U4/U6{middle dot}U5 tri-snRNP, functions as a heat-sensitive interaction node that couples spliceosome assembly to NS organization and splicing robustness under stress conditions.

plant biology↗

TCF4 induces enzalutamide resistance via neuroendocrine differentiation in prostate cancer

In treating patients with castration resistant prostate cancer (CRPC), enzalutamide, the second-generation androgen receptor (AR) antagonist, is an accepted standard of care. However, clinical benefits are limited to a median time of 4.8 months because resistance inevitably emerges. To determine the mechanism of treatment resistance, we carried out a RNA sequence analysis and found increased expression levels of neuroendocrine markers in the enzalutamide-resistant LNCaP human prostate cancer (CaP) cell line when compared to the parental cell line. Subsequent studies demonstrated that TCF4, a transcription factor implicated in Wnt signaling, mediated neuroendocrine differentiation (NED) in response to enzalutamide treatment and was elevated in the enzalutamide-resistant LNCaP. In addition, we observed that PTHrP mediated enzalutamide resistance in tissue culture and inducible TCF4 overexpression resulted in enzalutamide-resistance in a mouse xenograft model. Finally, small molecule inhibitors of TCF4 or PTHrP partially reversed enzalutamide resistance in CaP cells. When tissues obtained from men who died of metastatic CaP were examined, a positive correlation was found between the expression levels of TCF4 and PTHrP. Taken together, the current results indicate that TCF4 induces enzalutamide resistance via NED in CaP.

cancer biology↗