Beate Schwer

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Professor

Weill Cornell Medical College

United States

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About

Beate Schwer is a Professor at Weill Cornell Medical College in the United States. Her research focuses on inositol pyrophosphate catabolism, phosphate starvation responses in fission yeast, and the genetic interactions involved in transcriptional regulation. Recent publications highlight her work on functional redundancies among inositol pyrophosphatases and the genetic mechanisms underlying inositol pyrophosphate toxicosis.

Recent Grants

Grant: Close

Inositol pyrophosphate dynamics affect RNA 3'-processing/transcription termination

Open Date: 2019-08-01

Close Date: 2023-04-30

Grant: Close

RNA caps and meiotic pre-mRNA splicing

Open Date: 2013-06-07

Close Date: 2018-02-28

Grant: Close

Deciphering the RNA Polymerase II CTD Code

Open Date: 1995-05-01

Close Date: 2020-01-31

Grant: Close

Structure-Function Analysis of Spliceosomal ATPases

Open Date: 1994-01-01

Close Date: 2012-05-31

Articles (8)

Year:

2025

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2025

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2024

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2024

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2024

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2021

Year:

2020

Year:

2020

Collaborators (1)

Henning Jessen

Professor of Bioorganic Chemistry

University of Freiburg

GERMANY

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Beate Schwer

Research Interests

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About

Recent Grants

Articles (8)

Tandem inactivation of inositol pyrophosphatases Asp1, Siw14, and Aps1 illuminates functional redundancies in inositol pyrophosphate catabolism in fission yeast.

Efn1 and Efn2 are extracellular 5'-nucleotidases induced during the fission yeast response to phosphate starvation

Activities and genetic interactions of fission yeast Aps1, a Nudix-type inositol pyrophosphatase and inorganic polyphosphatase.

Suppression of inositol pyrophosphate toxicosis and hyper-repression of the fission yeast PHO regulon by loss-of-function mutations in chromatin remodelers Snf22 and Sol1

Genetic suppressor screen identifies Tgp1 (glycerophosphocholine transporter), Kcs1 (IP 6 kinase), and Plc1 (phospholipase C) as determinants of inositol pyrophosphate toxicosis in fission yeast

Genetic screen for suppression of transcriptional interference identifies a gain-of-function mutation in Pol2 termination factor Seb1

A genetic screen for suppressors of hyper-repression of the fission yeast PHO regulon by Pol2 CTD mutation T4A implicates inositol 1-pyrophosphates as agonists of precocious lncRNA transcription termination.

Genetic interactions and transcriptomics implicate fission yeast CTD prolyl isomerase Pin1 as an agent of RNA 3' processing and transcription termination that functions via its effects on CTD phosphatase Ssu72.

Collaborators (1)

Henning Jessen

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