Key stages of mammary gland development: Molecular mechanisms involved in the formation of the embryonic mammary gland

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Abstract

The development of the embryonic mammary gland involves communication between the epidermis and mesenchyme and is coordinated temporally and spatially by various signaling pathways. Although many more genes are likely to control mammary gland development, functional roles have been identified for Wnt, fibroblast growth factor, and parathyroid hormone-related protein signaling. This review describes what is known about the molecular mechanisms that regulate embryonic mammary gland development.

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Development of several organs that require inductive epithelial-mesenchymal interactions is impaired in LEF-1-deficient mice.

C van Genderen, R M Okamura, I Fariñas … (1994)

Lymphoid enhancer factor 1 (LEF-1) is a sequence-specific DNA-binding protein that is expressed in pre-B and T lymphocytes of adult mice, and in the neural crest, mesencephalon, tooth germs, whisker follicles, and other sites during embryogenesis. We have generated mice carrying a homozygous germ-line mutation in the LEF-1 gene that eliminates its protein expression and causes postnatal lethality. The mutant mice lack teeth, mammary glands, whiskers, and hair but show no obvious defects in lymphoid cell populations at birth. The LEF-1-deficient mice also lack the mesencephalic nucleus of the trigeminal nerve, the only neural crest-derived neuronal populations. Together, the pattern of these defects suggest an essential role for LEF-1 in the formation of several organs and structures that require inductive tissue interactions.

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Msx2 deficiency in mice causes pleiotropic defects in bone growth and ectodermal organ formation.

M Uchiyama, T Maeda, S Heaney … (2000)

The composite structure of the mammalian skull, which forms predominantly via intramembranous ossification, requires precise pre- and post-natal growth regulation of individual calvarial elements. Disturbances of this process frequently cause severe clinical manifestations in humans. Enhanced DNA binding by a mutant MSX2 homeodomain results in a gain of function and produces craniosynostosis in humans. Here we show that Msx2-deficient mice have defects of skull ossification and persistent calvarial foramen. This phenotype results from defective proliferation of osteoprogenitors at the osteogenic front during calvarial morphogenesis, and closely resembles that associated with human MSX2 haploinsufficiency in parietal foramina (PFM). Msx2-/- mice also have defects in endochondral bone formation. In the axial and appendicular skeleton, post-natal deficits in Pth/Pthrp receptor (Pthr) signalling and in expression of marker genes for bone differentiation indicate that Msx2 is required for both chondrogenesis and osteogenesis. Consistent with phenotypes associated with PFM, Msx2-mutant mice also display defective tooth, hair follicle and mammary gland development, and seizures, the latter accompanied by abnormal development of the cerebellum. Most Msx2-mutant phenotypes, including calvarial defects, are enhanced by genetic combination with Msx1 loss of function, indicating that Msx gene dosage can modify expression of the PFM phenotype. Our results provide a developmental basis for PFM and demonstrate that Msx2 is essential at multiple sites during organogenesis.

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Mutations in human TBX3 alter limb, apocrine and genital development in ulnar-mammary syndrome.

Albert Schinzel, Michael J. Bamshad, Benoit G. Bruneau … (1997)

Ulnar-mammary syndrome is a rare pleiotropic disorder affecting limb, apocrine gland, tooth and genital development. We demonstrate that mutations in human TBX3, a member of the T-box gene family, cause ulnar-mammary syndrome in two families. Each mutation (a single nucleotide deletion and a splice-site mutation) is predicted to cause haploinsufficiency of TBX3, implying that critical levels of this transcription factor are required for morphogenesis of several organs. Limb abnormalities of ulnar-mammary syndrome involve posterior elements. Mutations in TBX5, a related and linked gene, cause anterior limb abnormalities in Holt-Oram syndrome. We suggest that during the evolution of TBX3 and TBX5 from a common ancestral gene, each has acquired specific yet complementary roles in patterning the mammalian upper limb.

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Author and article information

Journal

Journal ID (nlm-ta): Breast Cancer Res

Title: Breast Cancer Research

Publisher: BioMed Central (London )

ISSN (Print): 1465-5411

ISSN (Electronic): 1465-542X

Publication date (Print): 2005

Publication date (Electronic): 10 August 2005

Volume: 7

Issue: 5

Pages: 220-224

Affiliations

[1 ]Section of Endocrinology and Metabolism, Department of Internal Medicine, Yale University School of Medicine, and Anlyan Center for Medical Research and Education, New Haven, Connecticut, USA

Article

Publisher ID: bcr1306

DOI: 10.1186/bcr1306

PMC ID: 1242158

PubMed ID: 16168142

SO-VID: e65cd9cf-db47-4425-b07c-cac7cf73f7d3

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Key stages of mammary gland development: Molecular mechanisms involved in the formation of the embryonic mammary gland

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Most cited references 20

Development of several organs that require inductive epithelial-mesenchymal interactions is impaired in LEF-1-deficient mice.

Msx2 deficiency in mice causes pleiotropic defects in bone growth and ectodermal organ formation.

Mutations in human TBX3 alter limb, apocrine and genital development in ulnar-mammary syndrome.

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