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Raz

Bar-Ziv

aging -  neurobiology -  gene regulation

Raz Bar-Ziv_JPG.jpg
WHO I AM

I'm a postdoctoral researcher at the department of Molecular and Cell Biology at UC Berkeley, working with Professor Andrew Dillin. I am broadly interested in the dynamics of protein homeostasis in the nervous system, in the context of aging and neurodegenerative diseases.  

I study the mechanisms responsible for the failure of protein homeostasis during aging in different tissues, with particular interest glia and neurons. I focus on revealing the mechanisms by which neurons and glia communicate within the nervous system, and to peripheral tissues, via the mitochondrial stress response. I combine genetic manipulations and microscopy, together with sequencing-based methods and metabolomics to tackle questions in neurodegeneration and aging. I am supported by The Larry L. Hillblom Foundation and the European Molecular Biology Organization.

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Transcription Factor Binding to Replicated DNA

Raz Bar-Ziv*, Sagie Brodsky*, Michal Chapal, Naama Barkai

(Cell Reports, 2020)

Genome replication perturbs the DNA regulatory environment by displacing DNA-bound proteins, replacing nucleosomes, and introducing dosage imbalance between regions replicating at different S-phase stages. Recently, we showed that these effects are integrated to maintain transcription homeostasis: replicated genes increase in dosage, but their expression remains stable due to replication-dependent epigenetic changes that suppress transcription. Here, we examine whether reduced transcription from replicated DNA results from limited accessibility to regulatory factors by measuring the time-resolved binding of RNA polymerase II (Pol II) and specific transcription factors (TFs) to DNA during S phase in budding yeast. We show that the Pol II binding pattern is largely insensitive to DNA dosage, indicating limited binding to replicated DNA. In contrast, binding of three TFs (Reb1, Abf1, and Rap1) to DNA increases with the increasing DNA dosage. We conclude that the replication-specific chromatin environment remains accessible to regulatory factors but suppresses RNA polymerase recruitment.

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