Cloning, sequencing, and expressional analysis of the chick homologue of follistatin

Connolly, David; Patel, Ketan; Seleiro, E. A. P.; Wilkinson, David G.; Cooke, Jonathan

doi:10.1002/dvg.1020170108

Cited by 52 publications

(25 citation statements)

References 32 publications

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“…In stage-12 − chicks, activin-␤B expression is detectable in notochord tissue but not in more lateral mesoderm (Fig. 4A), confirming previous work (Connolly et al 1995). Activin-␤A expression is not detected at this stage (Connolly et al 1995; data not shown).…”

Section: Notochord Factors Activin and Fgf Initiate Pancreatic Differsupporting

confidence: 89%

Notochord repression of endodermal Sonic hedgehog permits pancreas development

Hebrok

Kim²,

Melton³

1998

Genes Dev.

561

450

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Notochord signals to the endoderm are required for development of the chick dorsal pancreas. Sonic hedgehog (SHH) is normally absent from pancreatic endoderm, and we provide evidence that notochord, in contrast to its effects on adjacent neuroectoderm where SHH expression is induced, represses SHH expression in adjacent nascent pancreatic endoderm. We identify activin-␤B and FGF2 as notochord factors that can repress endodermal SHH and thereby permit expression of pancreas genes including Pdx1 and insulin. Endoderm treatment with antibodies that block hedgehog activity also results in pancreatic gene expression. Prevention of SHH expression in prepancreatic dorsal endoderm by intercellular signals, like activin and FGF, may be critical for permitting early steps of chick pancreatic development.

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Section: Notochord Factors Activin and Fgf Initiate Pancreatic Differsupporting

confidence: 89%

Notochord repression of endodermal Sonic hedgehog permits pancreas development

Hebrok

Kim²,

Melton³

1998

Genes Dev.

561

450

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“…Goldfish follistatin exhibits as much as 95% sequence identity with that of zebrafish (Bauer et al 1998) and about 75% with the homologous protein of other vertebrates (Inouye et al 1991, Tashiro et al 1991, Connolly et al 1995, suggesting conserved functions of this protein in vertebrates. In mammals and birds, Figure 5 Effects of recombinant human follistatin (100 ng/ml) and recombinant goldfish follistatin (50 ml/ml) on the expression of follistatin, FSHb, and LHb in the cultured pituitary cells.…”

Section: Discussionmentioning

confidence: 99%

Evidence for the existence of a local activin–follistatin negative feedback loop in the goldfish pituitary and its regulation by activin and gonadal steroids

Cheng¹,

Yuen²,

Ge³

2007

Journal of Endocrinology

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Activin is an important regulator of gonadotropin expression and production in the vertebrate pituitary, and its activity is fine-tuned by its binding protein follistatin. In the present study, a full-length cDNA for follistatin was cloned in the goldfish, which shows 74% amino acid sequence identity with that of mammals. Recombinant goldfish follistatin expressed in the Chinese hamster ovary cells significantly blocked activin-induced F5-5 cell differentiation. Goldfish follistatin is expressed in a wide range of tissues including the brain, pituitary, ovary, and testis. The expression of follistatin mRNA in the pituitary is regulated by both activin and gonadal steroids in vitro. Treatment with goldfish activin B for 48 h significantly up-regulated follistatin expression in cultured pituitary cells, suggesting a closed activin-follistatin feedback loop in the pituitary. In agreement with this, both human and goldfish follistatin down-regulated the expression of follistatin itself, probably due to the neutralization of endogenous activin. Examination of FSHb and LHb expression in the same samples supports the role of activin and follistatin in the differential regulation of FSH and LH as demonstrated previously. Since the expression level of activin b B in the pituitary is rather stable both in vitro and in vivo, it is conceivable that follistatin may play a pivotal regulatory role in the intra-pituitary activin system. Both estradiol and testosterone up-regulated follistatin expression in vitro, suggesting a mediating role for follistatin in steroid feedback on pituitary hormones. These results provide clues to the potential physiological roles of activin-follistatin system in the regulation of gonadotropin biosynthesis in teleosts.

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“…from the neural folds prior to NT closure and later from the roof plate). Among these are members of the TGFβ family, including activin, Bmp4 and Bmp7 (Connolly et al, 1995;Liem et al, 1997;Liem et al, 1995;Tam, 2001). The expression of these TGFβ family proteins in the neural plate at early developmental stages is in close proximity to migrating kidney IM precursor cells (James and Schultheiss, 2003) (Fig.…”

Section: Identifying the Source Tissue Of The Kidneyinductive Signalsmentioning

confidence: 99%

“…Activin is also expressed in the neural plate of stage 5-8 embryos (Connolly et al, 1995), which, at these stages, is in immediate contact with migrating kidney precursor cells. Limited evidence exists for the involvement of activin in early kidney induction.…”

Section: Activin-like Signaling Is Required But Insufficient For Kidnmentioning

confidence: 99%

Interplay between activin and Hox genes determines the formation of the kidney morphogenetic field

et al. 2009

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The kidney develops in a specific position along the anterior-posterior axis. All vertebrate kidney tissues are derived from the intermediate mesoderm (IM), and early kidney genes such as Lim1 and Pax2 are expressed in amniotes posterior to the sixth somite axial level. IM cells anterior to this level do not express kidney genes owing to changes in their competence to respond to kidneyinductive signals present along the entire axis. We aimed to understand the molecular mechanisms governing the loss of competence of anterior IM cells and the formation of the anterior border of the kidney morphogenetic field. We identified the dorsal neural tube as the potential kidney-inductive tissue and showed that activin, a secreted morphogen, is necessary but insufficient for Lim1 induction and establishment of the kidney field. Activin or activin-like and BMP signaling cascades are activated along the entire axis, including in anterior non-kidney IM, suggesting that competence to respond to these signals involves downstream or other components. Detailed expression pattern analysis of Hox genes during early chick development revealed that paralogous group four genes share the same anterior border as the kidney genes. Ectopic expression of Hoxb4 in anterior non-kidney IM, either by retinoic acid (RA) administration or plasmid-mediated overexpression, resulted in ectopic kidney gene expression. The anterior expansion of Lim1 expression was restrained when Hoxb4 was co-expressed with a truncated form of activin receptor. We suggest a model in which the competence of IM cells to respond to TGFβ signaling and express kidney genes is driven by RA and mediated by Hoxb4.

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Cloning, sequencing, and expressional analysis of the chick homologue of follistatin

Cited by 52 publications

References 32 publications

Notochord repression of endodermal Sonic hedgehog permits pancreas development

Notochord repression of endodermal Sonic hedgehog permits pancreas development

Evidence for the existence of a local activin–follistatin negative feedback loop in the goldfish pituitary and its regulation by activin and gonadal steroids

Interplay between activin and Hox genes determines the formation of the kidney morphogenetic field

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