<i>Pea3</i> expression is regulated by FGF signaling in developing retina

McCabe, Kathryn L.; McGuire, Christopher Roger; Reh, Thomas A.

doi:10.1002/dvdy.20631

Cited by 24 publications

(33 citation statements)

References 72 publications

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“…To our knowledge, this is one of very few studies of regulation of ETV genes by FGFs in mammals; Hasewaga et al demonstrated that FGF18 stimulated expression of ETV1, ETV4, and ETV5 in the mouse embryonic brain (Hasegawa et al, 2004). It has been stated that ETV4 is regulated by FGF in all (lower vertebrate) tissues studied (McCabe et al, 2006), but the present study suggests that this may only hold for non-mammalian vertebrates.…”

Section: Journal Of Cellular Physiologycontrasting

confidence: 45%

Fibroblast growth factor-2 regulation of sprouty and NR4A genes in bovine ovarian granulosa cells

et al. 2011

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Fibroblast growth factors (FGFs) alter ovarian function, at least in part by inhibiting steroid hormone secretion and affecting survival of granulosa cells. The mechanism of action of FGFs in ovarian follicle cells is largely unknown; in the present study we identified the major pathways used by FGF2 in non-luteinizing granulosa cells cultured under serum-free conditions. FGF2 increased abundance of mRNA encoding SPRY1, 2, and 4, but not SPRY3. Common pathways employed by FGF2 in the regulation of SPRY1, 2, and 4, as demonstrated by immunoblot and inhibitor studies, included ERK1/2 and Akt signaling. In contrast, PKC activation was necessary for FGF2-stimulated expression of SPRY1 and 4, but not for SPRY2. Intracellular calcium flux is critical and sufficient for SPRY2 expression, but not for SPRY1 and 4. We also identified the orphan nuclear receptor NR4A1 as a potential early response gene in FGF2 signaling, whose expression, like that of SPRY2, is critically dependent on calcium signaling. Together, these data identify FGF2-target genes in follicular granulosa cells, and demonstrate alternative pathway use for the differential control of SPRY genes.

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Section: Journal Of Cellular Physiologycontrasting

confidence: 45%

Fibroblast growth factor-2 regulation of sprouty and NR4A genes in bovine ovarian granulosa cells

et al. 2011

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“…This pattern continued at E10.5 (data not shown). Moreover, frontonasal expression of Spry1 and Pea3 , two Fgf8 -responsive genes (Brent and Tabin, 2004; Firnberg and Neubuser, 2002; McCabe et al, 2006; Minowanda et al, 1999; Roehl and Nusslein-Volhard, 2001), was highly reduced or lost by E10.5 in Fgf8 null/Neo embryos (Figure 4b, c). …”

Section: Resultsmentioning

confidence: 92%

Fgf8 dosage determines midfacial integration and polarity within the nasal and optic capsules

Griffin

Compagnucci

et al. 2013

Developmental Biology

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Craniofacial development requires an exquisitely timed and positioned cross-talk between the embryonic cephalic epithelia and mesenchyme. This cross-talk underlies the precise translation of patterning processes and information into distinct, appropriate skeletal morphologies. The molecular and cellular dialogue includes communication via secreted signaling molecules, including Fgf8, and effectors of their interpretation. Herein, we use genetic attenuation of Fgf8 in mice and perform gain-of-function mouse-chick chimeric experiments to demonstrate that significant character states of the frontonasal and optic skeletons are dependent on Fgf8. Notably, we show that the normal orientation and polarity of the nasal capsules and their developing primordia are dependent on Fgf8. We further demonstrate that Fgf8 is required for midfacial integration, and provide evidence for a role for Fgf8 in optic capsular development. Taken together, our data highlight Fgf8 signaling in craniofacial development as a plausible target for evolutionary selective pressures.

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“…FGF signaling may cooperate with Shh to coordinate the subsequent spread of RGC differentiation wave front. FGF19, via regulation of the Pea3 and Erm Ets-domain transcription factor genes, together with Shh released from new born RGCs, are required for propagation of Shh own gene expression (McCabe et al, 2006;Vinothkumar et al, 2008). Mutations in Shh signaling components and cyclopamine treatment all disrupt normal propagation of Shh and Atoh7 expression as well as RGC differentiation (Neumann and Nuesslein-Volhard, 2000;Stenkamp and Frey, 2003).…”

Section: Extrinsic Signalingmentioning

confidence: 99%