Placental failure in mice lacking the mammalian homolog of glial cells missing, GCMa.

Abstract:

:The GCM family of transcription factors consists of Drosophila melanogaster GCM, an important regulator of gliogenesis in the fly, and its two mammalian homologs, GCMa and GCMb. To clarify the function of these mammalian homologs, we deleted GCMa in mice. Genetic ablation of murine GCMa (mGCMa) is embryonic lethal, with mice dying between 9.5 and 10 days postcoitum. At the time of death, no abnormalities were apparent in the embryo proper. Nervous system development, in particular, was not impaired, as might have been expected in analogy to Drosophila GCM. Instead, placental failure was the cause of death. In agreement with the selective expression of mGCMa in labyrinthine trophoblasts, mutant placentas did not develop a functional labyrinth layer, which is necessary for nutrient and gas exchange between maternal and fetal blood. Only a few fetal blood vessels entered the placenta, and these failed to thrive and branch normally. Labyrinthine trophoblasts did not differentiate. All other layers of the placenta, including spongiotrophoblast and giant cell layer, formed normally. Our results indicate that mGCMa plays a critical role in trophoblast differentiation and the signal transduction processes required for normal vascularization of the placenta.

journal_name

Mol Cell Biol

authors

Schreiber J,Riethmacher-Sonnenberg E,Riethmacher D,Tuerk EE,Enderich J,Bösl MR,Wegner M

doi

10.1128/mcb.20.7.2466-2474.2000

subject

Has Abstract

pub_date

2000-04-01 00:00:00

pages

2466-74

issue

7

eissn

0270-7306

issn

1098-5549

journal_volume

20

pub_type

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