• Users Online: 826
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Contacts Login 
Year : 2021  |  Volume : 41  |  Issue : 1  |  Page : 29-37

The bHLH transcription factor E protein negatively regulates endoreplication in the salivary gland cells

1 Department of Medicine, National Defense Medical Center, Taipei, Taiwan
2 Department of Biochemistry, National Defense Medical Center, Taipei, Taiwan
3 Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan

Correspondence Address:
Dr. Lan-Hsin Wang
Graduate Institute of Life Sciences, National Defense Medical Center, Taipei
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jmedsci.jmedsci_128_20

Rights and Permissions

Background: Endoreplication is a variant cell cycle which generates massive DNA replication with no features of mitosis. In addition to abnormal occurrence of endoreplication in cancer cells, it is often found in plants and many different animal organs, such as liver, placenta, and Drosophila larval tissues. In treatment with anti-mitotic drugs, it has been shown that cancer cells may undergo endoreplication to escape apoptosis. However, the underlying mechanisms of endoreplication in normal and pathological circumstances remain obscure. Methods: The regulation and function of most physiological processes are highly conserved between the fruit fly Drosophila melanogaster and mammals. In addition, using Drosophila as a research model can largely reduce genetic redundancy issues and provide a suitable way to observe cell autonomy. To address the aforementioned questions, we use the Drosophila as an animal model to study the function of fundamental regulators in endoreplication. Results: In the present study, we demonstrated that high levels of bHLH transcription factor E protein are capable of inhibiting endoreplication in larval salivary glands. The negative regulation of E protein in endoreplication depends on the dysregulation of cell cycle regulators, including E2f1 and its target genes Cyclin E and PCNA. However, the endoreplication defects caused by E protein overexpression are independent of the Hippo tumor suppressor pathway. Conclusions: Our results reveal that endoreplication can be prevented by high levels of E protein through disrupting the oscillations of cell cycle regulators.

Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded69    
    Comments [Add]    

Recommend this journal