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Yeast sirutin family members maintain trannscription homeostasis to ensure genome stability

ABSTRACT: Yeast sirutin family members maintain trannscription homeostasis to ensure genome stability

PROVIDER: PRJNA510821 | ENA |

REPOSITORIES: ENA

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Yeast Sirtuin Family Members Maintain Transcription Homeostasis to Ensure Genome Stability.

Project description: Not available

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Yeast sirutin family members maintain trannscription homeostasis to ensure genome stability

Project description:Loss of Hst3 and Hst4 leads to increased nascent transcription which increases the prevelance of R-loops and contributes to DNA damage phenotype of the mutant

2019-05-04 | GSE124132 | GEO

p53 family members in myogenic differentiation and rhabdomyosarcoma development

Project description:The p53 family comprises the tumor suppressor p53 and the structural homologs p63 and p73. How the three family members cooperate in tumor suppression remains unclear. Here, we report different but complementary functions of the individual members for regulating retinoblastoma protein (RB) function during myogenic differentiation. Whereas p53 transactivates the retinoblastoma gene, p63 and p73 induce the cyclin-dependent kinase inhibitor p57 to maintain RB in an active, hypophosphorylated state. DeltaNp73 inhibits these functions of the p53 family in differentiation control, prevents myogenic differentiation, and enables cooperating oncogenes to transform myoblasts to tumorigenicity. DeltaNp73 is frequently overexpressed in rhabdomyosarcoma and essential for tumor progression in vivo. These findings establish differentiation control as a key tumor suppressor activity of the p53 family. Keywords: oligonucleotide

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The effect on lincRNA expression by p53 family members.

2014-02-05 | GSE52739 | GEO

The effect on lincRNA expression by p53 family members.

Project description:To evaluate the effect on lincRNA expression by p53 family members, we overexpressed p53 family members in H1299 cells and evaluated the lincRNA expression by microarray analysis. lincRNA expression was measured in H1299 cells infected with adenovirus expressing LacZ, p53, p63a, p63g, p73a and p73b.

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GATA Family Members as Inducers for Cellular Reprogramming to Pluripotency

Project description:Members of the GATA protein family play important roles in lineage specification and transdifferentiation. Previous reports show that some members of GATA protein family also can induce pluripotency in somatic cells by substituting for the key pluripotency-associated factor Oct4. However, the mechanism that links the lineage specifying cues and activation of pluripotency remains elusive. Here, we report that all GATA family members can substitute for Oct4 to induce pluripotency. We found that all members of the GATA family can inhibit elevated ectodermal-lineage genes, which is consistent with previous reports that a balance of different lineage-specifying forces is important for restoration of pluripotency. A conserved DNA-binding domain in the C-terminal zinc finger is critical for the GATA family to induce pluripotency. Using RNA-seq and ChIP-seq we identified that the pluripotency-related gene Sall4 is a direct target of GATA family members during reprogramming, serving as a bridge linking the lineage-specific GATA family to the pluripotency circuit. Thus, the GATA family is the first family of proteins wherein all members can function as inducers of the reprogramming process that can substitute for Oct4. Our results suggest that the roles of the GATA family in reprogramming have been greatly underestimated, and that the GATA family may serve as a general mediator for cell fate conversion.

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Sinorhizobium meliloti CspA family members mediate stability of structured sRNAs contributing to stress adaptation and effective symbiosis with alfalfa

Project description:Sinorhizobium meliloti CspA family members mediate stability of structured sRNAs contributing to stress adaptation and effective symbiosis with alfalfa

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Autophagy lipidation machinery regulates microtubule dynamics to maintain axonal homeostasis

Project description:Axon integrity is crucial for neuronal function. To maintain axonal homeostasis neurons have evolved a unique organization of the microtubule (MT) cytoskeleton, which supports axonal morphology and provides tracks for intracellular transport. Although abnormal MT-based trafficking highlights the pathology of neurodegenerative diseases, the exact mechanism regulating MT dynamics in the axon remains enigmatic. Here we report on a novel regulation of MT dynamics by autophagy, the pathway, which previously has been linked to lysosomal degradation. We find that AuTophaGy(ATG)-related proteins required for LC3 lipid conjugation regulate MT stability via controlling the abundance of MT-binding protein CLASP2. This function of ATGs is independent of their role in protein degradation and requires the active zone protein ELKS1. Our results highlight a novel role of autophagy in neurons and suggest that pharmacological activation of autophagy may not only promote the degradation of bulk cytoplasmic material, but also impair axonal integrity via altering the MT stability.

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ALBA protein complex reads genic R-loops to maintain genome stability in Arabidopsis

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Nucleoporin Seh1 Maintain Schwann Cell Homeostasis by Regulating Genome Stability and Necroptosis

Project description:Schwann cells play critical roles in peripheral neuropathies, however, the regulatory mechanisms of their homeostasis remain largely unknown. Here we show that nucleoporin Seh1, a component of nuclear pore complex, is important for Schwann cell homeostasis and loss of Seh1 led to necroptosis of non-myelinating Schwann cell and degeneration of sensory neurons. While myelinogenesis, myelinating Schwann cell, and wrapped large fibers were not affected, mice with depletion of Seh1 in Schwann cell lineage developed progressive reduction of non-myelinating Schwann cells in sciatic nerves, followed by the degeneration of unmyelinated small sensory fibers and malfunction of the sensory system. Mechanistically, Seh1 safeguards genome stability by mediating the interaction between SETDB1 and KAP1. The disrupted interaction after ablation of Seh1 derepresses endogenous retroviruses, which triggers ZBP1-dependent necroptosis in non-myelinating Schwann cells. Collectively, our results reveal that Seh1 is required for homeostasis of Schwann cells and suggest that decrease of nucleoporins as aging may participate in the pathogenesis of periphery neuropathies.

2023-01-03 | GSE222015 | GEO

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