Morgan Royce-Tolland

University of California, San Francisco

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Barbara Panning

University of California, San Francisco

Mary Kate Alexander

Kalasalingam Academy of Research and Education

Susanna Mlynarczyk‐Evans

Stanford University

Sundeep Kalantry

University of Michigan–Ann Arbor

Angela A. Andersen

University of California, San Francisco

Terry Magnuson

University of North Carolina at Chapel Hill

Alex Plocik

Ginkgo BioWorks (United States)

Joost Gribnau

Erasmus University Rotterdam

Hannah Cohen

University College London

Hannah R Koyfman

University of California, San Francisco

Cooperative Institutions

University of California, San Francisco

Whitehead Institute for Biomedical Research

Massachusetts Institute of Technology

Howard Hughes Medical Institute

University of North Carolina at Chapel Hill

University of Toronto

King's College London

UNC Lineberger Comprehensive Cancer Center

Harvard University

Brigham and Women's Hospital

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Investigation into the Molecular Mechanisms that Control Random X Chromosome Inactivation

Morgan Royce-Tolland

Author(s): Royce-Tolland, Morgan Elizabeth | Advisor(s): Panning, Barbara | Abstract: In eutherian mammals, dosage compensation between XX females and XY males is achieved by the transcriptional silencing of one X-chromosome in each female cell. The choice of which chromosome will be silenced is random in that both X chromosomes have an equal probability of being silenced. Despite nearly fifty years of research, the mechanisms that enable a cell to designate precisely one active and one inactive X chromosome remain elusive. What follows is an investigation into how X chromosomal fate is assigned. I present evidence that the two X chromosomes in a female cell adopt distinct states and that these states correlate with fate. I also explore the role of Xist's A-repeat in this process. The A-repeat is a highly conserved Xist element that is necessary for Xist-dependent silencing. The work within this thesis shows that the A-repeat is also required for random choice. I demonstrate that the A-repeat is important for post-transcriptional processing of Xist RNA and that the A-repeat binds the essential splicing factor ASF/SF2. In combination, these findings provide the foundation for a model in which regulation of Xist RNA splicing in ES cells is part of the stochastic process that determines which X will be inactivated in wild-type cells.

XIST

Dosage compensation

Skewed X-inactivation

Source

Cite

Citations (0)

X-Inactivation: It Takes Two to Count

Current Biology (2008)

Morgan Royce-Tolland Barbara Panning

Chromosome pairing

10.1016/j.cub.2008.01.039

Cite

Citations (4)

X Chromosomes Alternate between Two States prior to Random X-Inactivation

Carolina Digital Repository (University of North Carolina at Chapel Hill) (2006)

Susanna Mlynarczyk‐Evans Morgan Royce-Tolland Mary Kate Alexander Angela A. Andersen Sundeep Kalantry

10.17615/3r76-f463

Cite

Citations (0)

X Chromosomes Alternate between Two States prior to Random X-Inactivation

PLoS Biology (2006)

Susanna Mlynarczyk‐Evans Morgan Royce-Tolland Mary Kate Alexander Angela A. Andersen Sundeep Kalantry

Early in the development of female mammals, one of the two X chromosomes is silenced in half of cells and the other X chromosome is silenced in the remaining half. The basis of this apparent randomness is not understood. We show that before X-inactivation, the two X chromosomes appear to exist in distinct states that correspond to their fates as the active and inactive X chromosomes. Xist and Tsix, noncoding RNAs that control X chromosome fates upon X-inactivation, also determine the states of the X chromosomes prior to X-inactivation. In wild-type ES cells, X chromosomes switch between states; among the progeny of a single cell, a given X chromosome exhibits each state with equal frequency. We propose a model in which the concerted switching of homologous X chromosomes between mutually exclusive future active and future inactive states provides the basis for the apparently random silencing of one X chromosome in female cells.

XIST

Dosage compensation

10.1371/journal.pbio.0040159

Cite

Citations (65)

The A-repeat links ASF/SF2-dependent Xist RNA processing with random choice during X inactivation

Nature Structural & Molecular Biology (2010)

Morgan Royce-Tolland Angela A. Andersen Hannah R Koyfman Dale Talbot Anton Wutz

XIST

10.1038/nsmb.1877

Cite

Citations (91)

Differences between homologous alleles of olfactory receptor genes require the Polycomb Group protein Eed

The Journal of Cell Biology (2007)

Mary Kate Alexander Susanna Mlynarczyk‐Evans Morgan Royce-Tolland Alex Plocik Sundeep Kalantry

Anumber of mammalian genes are expressed from only one of the two homologous chromosomes, selected at random in each cell. These include genes subject to X-inactivation, olfactory receptor (OR) genes, and several classes of immune system genes. The means by which monoallelic expression is established are only beginning to be understood. Using a cytological assay, we show that the two homologous alleles of autosomal random monoallelic loci differ from each other in embryonic stem (ES) cells, before establishment of monoallelic expression. The Polycomb Group gene Eed is required to establish this distinctive behavior. In addition, we found that when Eed mutant ES cells are differentiated, they fail to establish asynchronous replication timing at OR loci. These results suggest a common mechanism for random monoallelic expression on autosomes and the X chromosome, and implicate Eed in establishing differences between homologous OR loci before and after differentiation.

10.1083/jcb.200706053

Cite

Citations (34)

An X-to-autosome retrogene is required for spermatogenesis in mice

Nature Genetics (2004)

Julie A. Bradley Andrew E. Baltus Helen Skaletsky Morgan Royce-Tolland Ken Dewar

Coding region

10.1038/ng1390

Cite

Citations (106)

Differences between homologous alleles of olfactory receptor genes require the Polycomb Group protein Eed

Carolina Digital Repository (University of North Carolina at Chapel Hill) (2007)