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在细胞自主因子df中存在缺陷的垂体前叶细胞会经历细胞谱系特化,但不会增殖。

Anterior pituitary cells defective in the cell-autonomous factor, df, undergo cell lineage specification but not expansion.

作者信息

Gage P J, Roller M L, Saunders T L, Scarlett L M, Camper S A

机构信息

Department of Human Genetics, University of Michigan Medical School, Medical Science II M3816, Ann Arbor 48109-0618, USA.

出版信息

Development. 1996 Jan;122(1):151-60. doi: 10.1242/dev.122.1.151.

DOI:10.1242/dev.122.1.151
PMID:8565826
Abstract

The Ames dwarf mouse transmits a recessive mutation (df) resulting in a profound anterior pituitary hypocellularity due to a general lack of thyrotropes, somatotropes and lactotropes. These cell types are also dependent on the pituitary-specific transcription factor, Pit-1. We present evidence that expression of Pit-1 and limited commitment to these cells lineages occurs in df/df pituitaries. Thus, the crucial role of df may be in lineage-specific proliferation, rather than cytodifferentiation. The presence of all three Pit-1-dependent cell types in clonally derived clusters provides compelling evidence that these three lineages share a common, pluripotent precursor cell. Clusters containing different combinations of Pit-1-dependent cell types suggests that the Pit-1+ precursor cells choose from multiple developmental options during ontogeny. Characterization of df/df<-->+/+ chimeric mice demonstrated that df functions by a cell-autonomous mechanism. Therefore, df and Pit-1 are both cell-autonomous factors required for thyrotrope, somatotrope and lactotrope ontogeny, but their relative roles are different.

摘要

艾姆斯侏儒小鼠携带一种隐性突变(df),由于普遍缺乏促甲状腺激素细胞、生长激素细胞和催乳激素细胞,导致垂体前叶细胞显著减少。这些细胞类型也依赖于垂体特异性转录因子Pit-1。我们提供的证据表明,Pit-1的表达以及对这些细胞谱系的有限定向分化发生在df/df垂体中。因此,df的关键作用可能在于谱系特异性增殖,而非细胞分化。在克隆衍生的细胞簇中存在所有三种依赖Pit-1的细胞类型,这提供了令人信服的证据,表明这三个谱系共享一个共同的多能前体细胞。包含不同组合的依赖Pit-1细胞类型的细胞簇表明,Pit-1+前体细胞在个体发育过程中可从多种发育选项中进行选择。对df/df<-->+/+嵌合小鼠的特征分析表明,df通过细胞自主机制发挥作用。因此,df和Pit-1都是促甲状腺激素细胞、生长激素细胞和催乳激素细胞个体发育所需的细胞自主因子,但它们的相对作用有所不同。

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Development. 1996 Jan;122(1):151-60. doi: 10.1242/dev.122.1.151.
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