Feinberg
Northwestern Medicine | Northwestern University | Faculty Profiles

News Center

  • Categories
    • Campus News
    • Disease Discoveries
    • Clinical Breakthroughs
    • Education News
    • Scientific Advances
  • Press Releases
  • Media Coverage
  • Podcasts
  • Editor’s Picks
    • COVID-19
    • Cardiology
    • Cancer
    • Neurology and Neuroscience
    • Aging and Longevity
    • Artificial Intelligence in Medicine
  • News Archives
  • About Us
    • Media Contact
    • Share Your News
    • News Feeds
    • Social Media
    • Contact Us
Menu
  • Categories
    • Campus News
    • Disease Discoveries
    • Clinical Breakthroughs
    • Education News
    • Scientific Advances
  • Press Releases
  • Media Coverage
  • Podcasts
  • Editor’s Picks
    • COVID-19
    • Cardiology
    • Cancer
    • Neurology and Neuroscience
    • Aging and Longevity
    • Artificial Intelligence in Medicine
  • News Archives
  • About Us
    • Media Contact
    • Share Your News
    • News Feeds
    • Social Media
    • Contact Us
Home » Uncovering a Novel Mechanism in Cell Division
Scientific Advances

Uncovering a Novel Mechanism in Cell Division

By Sarah PlumridgeApr 17, 2017
Share
Facebook Twitter Email
In cancer cells, defects in the bipolar spindle leads to pulling chromosomes in multiple directions during cell division.
In cancer cells, defects in the bipolar spindle lead to pulling chromosomes in multiple directions during cell division.

Northwestern Medicine scientists have revealed the role amino-terminal methylation plays in a specific protein in the centromere, a region of the chromosome important in cell division, and how the dysregulation of this protein can affect the development of cancer cells. Methylation of amino acid side chains is well-documented, but the role of amino-terminal methylation is much less well understood.

Published in Nature Communications, the study showed this posttranslational modification of the protein, centromere protein A (CENP-A), distinguishes it from a similar protein that is found in the rest of the chromosome. CENP-A is a type of histone, a protein with DNA wrapped around it, and specifies the location of the centromere in the nucleus.

Lead author Daniel Foltz, ’01 PhD, associate professor of Biochemistry and Molecular Genetics, and his team conducted functional analyses of the modifications on CENP-A, which they had previously identified.

“It’s interesting because this is a novel type of modifications on histones and because we can go in and really show what function is being mediated by the amino-terminal methylation, which has not been previously well-defined for this type of modification,” Foltz said.

The investigators discovered that CENP-A, when correctly methylated on its amino terminus, influences the recruitment of CCAN proteins, which are part of a large centromere complex of proteins. They showed that a subset of components of CCAN are dependent on this methylation. When the scientists blocked methylation from this process, they observed defects in chromosome segregation.

“We really defined a different arm of recruitment for the CCAN proteins than has been understood before,” Foltz said.

Overexpression of CENP-A in Cancer

Next, the scientists studied hallmarks of cancer cells, including defects in chromosome segregation and spindle polarity. A bipolar spindle is essential to equally segregate chromosomes into two separate cells during cell division. In cancer cells, defects in the spindle lead to chromosomes that are pulled in multiple directions and can result in chromosome breakage and genomic instability. The scientists found that reducing the amount of methylation of CENP-A drives this process.

Foltz and the other investigators also found that in the absence of the tumor suppressor protein p53, loss of CENP-A methylation promotes more rapid tumor formation.

Next, Foltz and his team want to study how tumor cells are using this pathway.

“What we’ve done in this paper is engineer this defect into cells to see what the phenotype is,” Foltz said. “The next question is what happens to CENP-A methylation in cancer cells, and when CENP-A is overexpressed, to what degree is it driving the genomic instability in cancers?”

Foltz is also a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

The study was funded by Department of Defense Visionary Postdoctoral Fellowship W81XWH-13-1-0106, National Institutes of Health grant R01GM111907 and a research scholar award from the American Cancer Society.

Biochemistry Genetics Research
Share. Facebook Twitter Email

Related Posts

Pre-Surgery Immunotherapy May Increase Survival in Advanced Melanoma

Mar 23, 2023

Hormone Therapy Plus Current Treatments Improves Survival in Prostate Cancer

Mar 22, 2023

How ChatGPT Has, and Will Continue to, Transform Scientific Research

Mar 21, 2023

Comments are closed.

Latest News

Pre-Surgery Immunotherapy May Increase Survival in Advanced Melanoma

Mar 23, 2023

Hormone Therapy Plus Current Treatments Improves Survival in Prostate Cancer

Mar 22, 2023

How ChatGPT Has, and Will Continue to, Transform Scientific Research

Mar 21, 2023

New Directions for HIV Treatment

Mar 21, 2023

Humans are Not Just Big Mice: Identifying Science’s Muscle-Scaling Problem

Mar 20, 2023
  • News Center Home
  • Categories
  • Press Release
  • Media Coverage
  • Editor’s Picks
  • News Archives
  • About Us
Flickr Photos
20230315_NM036
20230315_NM046
20230315_NM134
20230315_NM205
20230315_NM206
20230315_NM132
20230315_NM130
20230315_NM082
20230315_NM063
20230315_NM058
20230315_NM030
20230315_NM038

Northwestern University logo

Northwestern University Feinberg School of Medicine

RSS Facebook Twitter LinkedIn Flickr YouTube Instagram
Copyright © 2023 Northwestern University
  • Contact Northwestern University
  • Disclaimer
  • Campus Emergency Information
  • Policy Statements

Type above and press Enter to search. Press Esc to cancel.