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      How to make a teleost adenohypophysis: Molecular pathways of pituitary development in zebrafish

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      Molecular and Cellular Endocrinology
      Elsevier BV

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          Abstract

          The anterior pituitary gland, or adenohypophysis (AH), represents the key component of the vertebrate hypothalamo-hypophyseal axis, where it functions at the interphase of the nervous and endocrine system to regulate basic body functions like growth, metabolism and reproduction. For developmental biologists, the adenohypophysis serves as an excellent model system for the studies of organogenesis and differential cell fate specification. Previous research, mainly done in mouse, identified numerous extrinsic signaling cues and intrinsic transcription factors that orchestrate the gland's developmental progression. In the past years, the zebrafish has emerged as a powerful tool to elucidate the genetic networks controlling vertebrate development, behavior and disease. Based on mutants isolated in forward genetic screens and on gene knock-downs using morpholino oligonucleotide (oligo) antisense technology, our current understanding of the molecular machinery driving adenohypophyseal ontogeny could be considerably improved. In addition, comparative analyses have shed further light onto the evolution of this rather recently invented organ. The goal of this review is to summarize current knowledge of the genetic and molecular control of zebrafish pituitary development, with special focus on most recent findings, including some thus far unpublished data from our own laboratory on the transcription factor Six1. In addition, zebrafish data will be discussed in comparison with current understanding of adenohypophysis development in mouse.

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          Author and article information

          Journal
          Molecular and Cellular Endocrinology
          Molecular and Cellular Endocrinology
          Elsevier BV
          03037207
          November 2009
          November 2009
          : 312
          : 1-2
          : 2-13
          Article
          10.1016/j.mce.2009.03.012
          19728983
          ef8a2d7a-c8cc-44c7-bb61-00b987ddf121
          © 2009

          https://www.elsevier.com/tdm/userlicense/1.0/

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