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The forkhead transcription factor, Foxd1, is necessary for pituitary luteinizing hormone expression in mice.

Gumbel JH, Patterson EM, Owusu SA, Kabat BE, Jung DO, Simmons J, Hopkins T, Ellsworth BS - PLoS ONE (2012)

Bottom Line: Loss of Foxd1 also results in significantly decreased levels of Lhb expression at e18.5.This decrease in Lhb expression does not appear to be due to a change in the number of gonadotrope cells in the pituitary gland.Previous studies have shown that loss of the LIM homeodomain factor, Lhx3, which is activated by the FGF signaling pathway, results in loss of LH production.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Southern Illinois University, Carbondale, Illinois, USA.

ABSTRACT
The pituitary gland regulates numerous physiological functions including growth, reproduction, temperature and metabolic homeostasis, lactation, and response to stress. Pituitary organogenesis is dependent on signaling factors that are produced in and around the developing pituitary. The studies described in this report reveal that the forkhead transcription factor, Foxd1, is not expressed in the developing mouse pituitary gland, but rather in the mesenchyme surrounding the pituitary gland, which is an essential source of signaling factors that regulate pituitary organogenesis. Loss of Foxd1 causes a morphological defect in which the anterior lobe of the pituitary gland protrudes through the cartilage plate that is developing ventral to the pituitary at embryonic days (e)14.5, e16.5, and e18.5. The number of proliferating pituitary cells is increased at e14.5 and e16.5. Loss of Foxd1 also results in significantly decreased levels of Lhb expression at e18.5. This decrease in Lhb expression does not appear to be due to a change in the number of gonadotrope cells in the pituitary gland. Previous studies have shown that loss of the LIM homeodomain factor, Lhx3, which is activated by the FGF signaling pathway, results in loss of LH production. Although there is a difference in Lhb expression in Foxd1 mice, the expression pattern of LHX3 is not altered in Foxd1 mice. These studies suggest that Foxd1 is indirectly required for normal Lhb expression and cartilage formation.

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Apoptosis is not different in Foxd1LacZ/LacZ embryos.TUNEL was performed to label apoptotic cells in mid-sagittal sections from Foxd1LacZ/LacZ embryos and wild type littermates. (A–F) No loss of apoptosis was observed. (A–B) Arrows indicate regions of pituitary cell apoptosis. Pictures were taken at 200X and scale bars represent 100 µm.
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pone-0052156-g005: Apoptosis is not different in Foxd1LacZ/LacZ embryos.TUNEL was performed to label apoptotic cells in mid-sagittal sections from Foxd1LacZ/LacZ embryos and wild type littermates. (A–F) No loss of apoptosis was observed. (A–B) Arrows indicate regions of pituitary cell apoptosis. Pictures were taken at 200X and scale bars represent 100 µm.

Mentions: Apoptosis and proliferation are essential processes for normal pituitary development. Apoptosis occurs at e10.5 to separate Rathke’s pouch from the oral ectoderm that will form the lining of the mouth [30]. After Rathke’s pouch is separated from the rest of the oral ectoderm, a cartilage plate forms to separate the pituitary from the oral cavity. If apoptosis fails to occur, the pituitary will remain attached to the rest of the oral ectoderm and the cartilage plate will not form completely [31]. To determine if failure of apoptosis caused the pituitary of Foxd1 embryos to protrude through the cartilage plate, apoptotic cells were labeled by TUNEL analysis. No significant difference in the number of apoptotic pituitary cells was detected in Foxd1 embryos as compared to wild type littermates (Fig. 5A–F). This suggests that the pituitary/cartilage dysmorphology in Foxd1 embryos is not due to a failure in apoptosis.


The forkhead transcription factor, Foxd1, is necessary for pituitary luteinizing hormone expression in mice.

Gumbel JH, Patterson EM, Owusu SA, Kabat BE, Jung DO, Simmons J, Hopkins T, Ellsworth BS - PLoS ONE (2012)

Apoptosis is not different in Foxd1LacZ/LacZ embryos.TUNEL was performed to label apoptotic cells in mid-sagittal sections from Foxd1LacZ/LacZ embryos and wild type littermates. (A–F) No loss of apoptosis was observed. (A–B) Arrows indicate regions of pituitary cell apoptosis. Pictures were taken at 200X and scale bars represent 100 µm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3526578&req=5

pone-0052156-g005: Apoptosis is not different in Foxd1LacZ/LacZ embryos.TUNEL was performed to label apoptotic cells in mid-sagittal sections from Foxd1LacZ/LacZ embryos and wild type littermates. (A–F) No loss of apoptosis was observed. (A–B) Arrows indicate regions of pituitary cell apoptosis. Pictures were taken at 200X and scale bars represent 100 µm.
Mentions: Apoptosis and proliferation are essential processes for normal pituitary development. Apoptosis occurs at e10.5 to separate Rathke’s pouch from the oral ectoderm that will form the lining of the mouth [30]. After Rathke’s pouch is separated from the rest of the oral ectoderm, a cartilage plate forms to separate the pituitary from the oral cavity. If apoptosis fails to occur, the pituitary will remain attached to the rest of the oral ectoderm and the cartilage plate will not form completely [31]. To determine if failure of apoptosis caused the pituitary of Foxd1 embryos to protrude through the cartilage plate, apoptotic cells were labeled by TUNEL analysis. No significant difference in the number of apoptotic pituitary cells was detected in Foxd1 embryos as compared to wild type littermates (Fig. 5A–F). This suggests that the pituitary/cartilage dysmorphology in Foxd1 embryos is not due to a failure in apoptosis.

Bottom Line: Loss of Foxd1 also results in significantly decreased levels of Lhb expression at e18.5.This decrease in Lhb expression does not appear to be due to a change in the number of gonadotrope cells in the pituitary gland.Previous studies have shown that loss of the LIM homeodomain factor, Lhx3, which is activated by the FGF signaling pathway, results in loss of LH production.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Southern Illinois University, Carbondale, Illinois, USA.

ABSTRACT
The pituitary gland regulates numerous physiological functions including growth, reproduction, temperature and metabolic homeostasis, lactation, and response to stress. Pituitary organogenesis is dependent on signaling factors that are produced in and around the developing pituitary. The studies described in this report reveal that the forkhead transcription factor, Foxd1, is not expressed in the developing mouse pituitary gland, but rather in the mesenchyme surrounding the pituitary gland, which is an essential source of signaling factors that regulate pituitary organogenesis. Loss of Foxd1 causes a morphological defect in which the anterior lobe of the pituitary gland protrudes through the cartilage plate that is developing ventral to the pituitary at embryonic days (e)14.5, e16.5, and e18.5. The number of proliferating pituitary cells is increased at e14.5 and e16.5. Loss of Foxd1 also results in significantly decreased levels of Lhb expression at e18.5. This decrease in Lhb expression does not appear to be due to a change in the number of gonadotrope cells in the pituitary gland. Previous studies have shown that loss of the LIM homeodomain factor, Lhx3, which is activated by the FGF signaling pathway, results in loss of LH production. Although there is a difference in Lhb expression in Foxd1 mice, the expression pattern of LHX3 is not altered in Foxd1 mice. These studies suggest that Foxd1 is indirectly required for normal Lhb expression and cartilage formation.

Show MeSH
Related in: MedlinePlus