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Updated: Apr 10, 2026
Loss- and Gain-of-function Approach to Investigate Early Cell Fate Determinants in Preimplantation Mouse Embryos
Published on: June 6, 2016
Loss of Foxm1 Results in Reduced Somatotrope Cell Number during Mouse Embryogenesis
Michael J Calderon1, Adam G Ploegman1, Brock Bailey1
1Department of Physiology, Southern Illinois University, Carbondale, Illinois, United States of America.
Abstract:
FOXM1, a member of the forkhead box transcription factor family, plays a key role in cell cycling progression by regulating the expression of critical G1/S and G2/M phase transition genes. In vivo studies reveal that Foxm1 null mice have a 91% lethality rate at e18.5 due to significant cardiovascular and hepatic hypoplasia. Thus, FOXM1 has emerged as a key protein regulating mitotic division and cell proliferation necessary for embryogenesis. In the current study, we assess the requirement for Foxm1 in the developing pituitary gland. We find that Foxm1 is expressed in the pituitary at embryonic days 10.5-e18.5 and localizes with markers for active cell proliferation (BrdU). Interestingly, direct analysis of Foxm1 null mice at various embryonic ages, reveals no difference in gross pituitary morphology or cell proliferation. We do observe a downward trend in overall pituitary cell number and a small reduction in pituitary size in e18.5 embryos suggesting there may be subtle changes in pituitary proliferation not detected with our proliferation makers. Consistent with this, Foxm1 null mice have reductions in both the somatotrope and gonadotrope cell populations.
Insights
Forkhead box protein M1 (FOXM1) is crucial for embryonic development, but its role in the pituitary gland is subtle. Foxm1 null mice show reduced somatotrope and gonadotrope cell populations, indicating a role in specific pituitary cell development.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- Forkhead box M1 (FOXM1) is a transcription factor vital for cell cycle progression and embryonic development.
- Foxm1 null mice exhibit embryonic lethality due to cardiovascular and hepatic defects, highlighting its critical role in embryogenesis.
Purpose of the Study:
- To investigate the role of Foxm1 in the development of the pituitary gland.
- To determine if Foxm1 is essential for pituitary cell proliferation and differentiation during embryogenesis.
Main Methods:
- Expression analysis of Foxm1 in the developing pituitary gland using embryonic day (e) 10.5-e18.5 embryos.
- Localization of Foxm1 with proliferation markers like BrdU.
- Phenotypic analysis of Foxm1 null mice pituitaries for morphology, cell proliferation, and cell populations.
Main Results:
- Foxm1 is expressed in the embryonic pituitary and co-localizes with proliferation markers.
- Foxm1 null mice do not show gross pituitary morphological defects or altered overall proliferation.
- A trend towards reduced pituitary cell number and size, with significant reductions in somatotrope and gonadotrope cell populations, was observed in Foxm1 null embryos.
Conclusions:
- While Foxm1 is not essential for overall pituitary development or proliferation, it plays a specific role in the development of somatotrope and gonadotrope cell lineages.
- These findings suggest a nuanced function for FOXM1 in regulating the differentiation or survival of specific endocrine cell types within the pituitary gland.
