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Biology subjects

Dang, H. Q.

Publications and source records attributed to Dang, H. Q..

4 recordsLinked to original sources

Somatic copy number mutations contribute to fitness in transplantation models of spontaneous human breast cancer metastasis

The contribution of somatic gene dosage mutations (CNA) to breast cancer metastasis remains poorly defined. Using 9 transplantable human neoadjuvant-naive triple-negative breast cancer xenografts, we studied the fitness of copy number clones in spontaneous metastasis from orthotopic transplant sites. Metastatic site preference was strongly patient-dependent, and the emergence of metastases exhibited a general trend toward slower growth at the orthotopic site. In our models, single-cell whole-genome sequencing of primary and metastatic sites showed that distant metastases were most often the result of minor prevalence clones at the orthotopic site, suggesting that some metastatic phenotypes may be weakly negatively fit at the primary site. We validated the existence of a fitness hierarchy of copy number clones using a previously established paradigm of remixing and retransplanting clones. Single-cell clone analysis of competitive repopulation and re-emergence of metastases showed that CNAs arising in cancer evolution can mediate metastatic fitness. Moreover, some clones displaying strong metastatic tendency exhibited weaker survival at the primary site, consistent with the notion that metastatic phenotypes could have a fitness cost at the primary site. Finally, we conducted RNA-seq analysis combined with DriverNet analysis to dissect the contribution of CNA-mediated versus genome-independent transcriptional states. CNA mutations appeared to contribute strongly to transcriptional differences between clones. Among clones of high metastatic potential, we observed CNA-mediated and CNA-independent convergence on pathways such as epithelial-mesenchymal transition (EMT), established as mediators of metastatic cell survival at distant sites. Taken together, our data point to a contribution of CNA-mediated cancer evolution to metastatic states and identify distant-site context as a key determinant of CNA-mediated fitness.

cancer biology↗

Default mode network spatio-temporal electrophysiological signature and causal role in creativity

The default mode network (DMN) is a widely distributed, intrinsic brain network thought to play a crucial role in internally-directed cognition. It subserves self-referential thinking, recollection of the past, mind wandering, and creativity. Knowledge about the electrophysiology underlying DMN activity is scarce, due to the difficulty to simultaneously record from multiple distant cortical areas with commonly-used techniques. The present study employs stereo-electroencephalography depth electrodes in 13 human patients undergoing monitoring for epilepsy, obtaining high spatiotemporal resolution neural recordings across multiple canonical DMN regions. Our results offer a rare insight into the temporal evolution and spatial origin of theta (4-8Hz) and gamma signals (30-70Hz) during two DMN-associated higher cognitive functions: mind-wandering and alternate uses. During the performance of these tasks, DMN activity is defined by a specific pattern of decreased theta coupled with increased gamma power. Critically, creativity and mind wandering engage the DMN with different dynamics: creativity recruits the DMN strongly during the covert search of ideas, while mind wandering displays the strongest modulation of DMN during the later recall of the train of thoughts. Theta band power modulations, predominantly occurring during mind wandering, do not show a predominant spatial origin within the DMN. In contrast, gamma power effects were similar for mind wandering and creativity and more strongly associated to lateral temporal nodes. Interfering with DMN activity through direct cortical stimulation within several DMN nodes caused a decrease in creativity, specifically reducing the originality of the alternate uses, without affecting creative fluency or mind wandering. These results suggest that DMN activity is flexibly modulated as a function of specific cognitive processes and supports its causal role in creative thinking. Our findings shed light on the neural constructs supporting creative cognition and provide causal evidence for the role of DMN in the generation of original connections among concepts.

neuroscience↗

Developmentally programmed switches in DNA replication: gene amplification and genome-wide endoreplication in Tetrahymena.

Locus-specific gene amplification and genome-wide endoreplication generate the elevated copy number of ribosomal DNA (rDNA, 9000 C) and non-rDNA (45 C) chromosomes in the developing macronucleus of Tetrahymena thermophila. Subsequently, all macronuclear chromosomes replicate once per cell cycle during vegetative growth. Here we describe an unanticipated, programmed switch in the regulation of replication initiation in the rDNA minichomosome. Early in development the 21 kb rDNA minichromosome is preferentially amplified from 2 C to ~800 C from well-defined origins, concurrent with genome-wide endoreplication (2 C to 8-16 C) in starved mating Tetrahymena (endoreplication (ER) Phase 1). Upon refeeding, rDNA and non-rDNA chromosomes achieve their final copy number through resumption of just the endoreplication program (ER Phase 2). Unconventional rDNA replication intermediates are generated primarily during ER phase 2, consistent with delocalized replication initiation and possible formation of persistent RNA-DNA hybrids. Origin usage and replication fork elongation are affected in non-rDNA chromosomes as well. Despite the developmentally programmed 10-fold reduction in the ubiquitous eukaryotic initiator, the Origin Recognition Complex (ORC), active initiation sites are more closely spaced in ER phases 1 and 2 compared to vegetative growing cells. We propose that initiation site selection is relaxed in endoreplicating macronuclear chromosomes and may be less dependent on ORC.

molecular biology↗

Single-molecule live cell imaging of the Smc5/6 DNA repair complex

The essential Smc5/6 complex is required in response to replication stress and is best known for ensuring the fidelity of homologous recombination. Using single-molecule tracking in live fission yeast to investigate Smc5/6 chromatin association, we show that Smc5/6 is chromatin associated in unchallenged cells and this depends on the non-SMC protein Nse6. We define a minimum of two Nse6-dependent sub-pathways, one of which requires the BRCT-domain protein Brc1. Using defined mutants in genes encoding the core Smc5/6 complex subunits we show that the Nse3 double-stranded DNA binding activity and the arginine fingers of the two Smc5/6 ATPase binding sites are critical for chromatin association. Interestingly, disrupting the ssDNA binding activity at the hinge region does not prevent chromatin association but leads to elevated levels of gross chromosomal rearrangements during replication restart. This is consistent with a downstream function for ssDNA binding in regulating homologous recombination.

molecular biology↗