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Phosphosite CGE assay

ABSTRACT: CGE analysis of proliferation associated phosphorylation

PROVIDER: PRJEB88223 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR14828865.fastq.gz	Fastqsanger.gz
	ERR14828866.fastq.gz	Fastqsanger.gz
	ERR14828867.fastq.gz	Fastqsanger.gz
	ERR14828868.fastq.gz	Fastqsanger.gz
	ERR14828869.fastq.gz	Fastqsanger.gz

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Project description:Reliable methods to quantify dynamic signaling changes across diverse pathways are needed to better understand the effects of disease and drug treatment in cells and tissues but are presently lacking. Here, we present SigPath, a targeted mass spectrometry (MS) assay that measures 284 phosphosites in 200 phosphoproteins of biological interest. SigPath probes a broad swath of signaling biology with high throughput and quantitative precision. We applied the assay to investigate changes in phospho-signaling in drug-treated cancer cell lines, breast cancer preclinical models, and human medulloblastoma tumors. In addition to validating previous findings, SigPath detected and quantified a large number of differentially regulated phosphosites newly associated with disease models and human tumors at baseline or with drug perturbation. Our results highlight the potential of SigPath to monitor phosphoproteomic signaling events and to nominate mechanistic hypotheses regarding oncogenesis, response, and resistance to therapy.

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Gene expression profile at single cell level of human cerebral cortical organoids with and without LIF treatment

Project description:Proper regulation of the proliferation and differentiation of radial glia (RG), the neural stem cells of the developing cortex, is fundamental for brain growth and organization. In humans, a specialized RG subtype, the outer radial glia (oRG), are abundant and give rise to diverse neuronal and glial progeny. However, the mechanisms regulating oRG development and differentiation are not fully understood. Here we investigated the regulation of oRG expansion and lineage potential by perturbing Leukemia Inhibitory Factor (LIF) signaling in the developing human cortex and in human pluripotent stem cell (PSC)-derived cortical organoids. LIF receptors are specifically expressed in oRG cells during neurogenesis, and, consistent with the previously described role of this cytokine as an activator of stem cell self-renewal, LIF treatment increased the number of oRG cells. Surprisingly, LIF treatment also increased the production of inhibitory interneurons (INs) in the cortex. Comparative transcriptomic analysis suggested that these INs resemble INs produced in the caudal ganglionic eminence (CGE). To test if oRG cells are the progenitors of these CGE-like INs, we isolated oRG cells from primary developing cortex and cultured them for several weeks with and without LIF treatment. We found that CGE-like INs were produced by oRG cells, and their abundance is increased by LIF treatment. Together, these observations suggest that LIF signaling regulates oRG lineage potential and capacity to generate CGE-like INs.

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A regulatory phosphosite on Mec1 controls RNAPII and RNAPIII occupancy during replication stress [tDNA]

Project description:Upon replication stress, the Mec1ATR kinase triggers the downregulation of transcription, reducing the level of RNA polymerase on chromatin to facilitate replication fork progression. We identify a hydroxyurea-induced phosphorylation site at Mec1-S1991 that contributes to the eviction of RNAPII and RNAPIII during replication stress. The non-phosphorylatable mec1-S1991A mutant reduces replication fork progression genome-wide and compromises survival on hydroxyurea. This defect can be suppressed by destabilizing chromatin-bound RNAPII with a Rpb3-TAP fusion, suggesting that lethality arises from replication-transcription conflicts. Coincident with a failure to repress gene expression, highly transcribed genes like GAL1 persist at nuclear pores in mec1-S1991A cells. Consistently, we find pore proteins and several components controlling RNAPII and RNAPIII transcription are phosphorylated in a Mec1-dependent manner, suggesting that Mec1-S1991 phosphorylation limits conflicts between replication and either RNA polymerase complex. We further show that Mec1 contributes to reduced RNAPII occupancy on chromatin during an unperturbed S phase.

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