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Updated: Aug 19, 2026
From MEFs to Matrigel I: Passaging hESCs in the Presence of MEFs
Published on: June 4, 2008
Effect of passaging on Mer phenotype of human fetal cell cultures
R S Day1, L H Honore, K D Dobler
1Department of Medicine, Cross Cancer Institute, Edmonton, Alb., Canada.
Abstract:
With increasing passage in culture, the human fibroblast cell strain GM11 lost the Mer+ phenotype (the ability to support the growth of adenovirus 5 damaged prior to infection by MNNG). All of 46 embryonic strains prepared either from various organs of 20 fetuses from 6-7 to 13-14 weeks of gestational age or from two hydatidiform moles showed normal repair of MNNG-treated virus. We conclude that human fetal strains are not usually deficient in such repair, and that the behavior of GM11 is atypical.
Insights
Human fetal cell strains typically repair MNNG-damaged adenovirus, unlike the GM11 fibroblast strain which loses this Mer+ phenotype with passaging. This suggests GM11
Area of Science:
- Cell biology
- Virology
- Genetics
Background:
- The Mer+ phenotype is crucial for supporting the growth of damaged adenovirus.
- Human fibroblast cell strain GM11 exhibits a loss of the Mer+ phenotype with increasing passage in culture.
Purpose of the Study:
- To investigate the viral repair capabilities of human fetal cell strains.
- To determine if the loss of the Mer+ phenotype in GM11 is a common characteristic of human fibroblasts or an atypical finding.
Main Methods:
- Preparation and culturing of 46 human embryonic fibroblast strains from fetal organs and hydatidiform moles.
- Assessment of the ability of these strains to support the growth of MNNG-damaged adenovirus 5, indicating viral repair capacity.
Main Results:
- All 46 human fetal fibroblast strains demonstrated normal repair of MNNG-treated adenovirus 5.
- The human fibroblast cell strain GM11, unlike the fetal strains, lost its Mer+ phenotype after extensive culturing.
Conclusions:
- Human fetal cell strains generally possess normal viral repair mechanisms.
- The atypical loss of the Mer+ phenotype in the GM11 cell strain is not representative of typical human fetal fibroblast behavior.
