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Gene Review

Foxd1  -  forkhead box D1

Mus musculus

Synonyms: AI385632, BF-2, Brain factor 2, FREAC-4, FREAC4, ...
 
 
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High impact information on Foxd1

  • BF-2 expression within the developing kidney is restricted to the stromal cell lineage [1].
  • Our findings demonstrate that BF-2 and stromal cells have essential functions during kidney morphogenesis [1].
  • The disruption of BF-2 reduces the rate of differentiation of the condensed mesenchyme into tubular epithelium, as well as the rate of growth and branching of the ureter and collecting system [1].
  • We have investigated the molecular and cellular basis of the kidney phenotypes displayed by Foxd1-null embryos and report here that they are likely to be caused by a failure in the correct formation of the renal capsule [2].
  • Foxd1 is required for proper formation of the optic chiasm [3].
 

Biological context of Foxd1

  • We report here that in embryos lacking Foxd1, both retinal development and chiasm morphogenesis are disrupted [3].
  • We show that BF-2 is a sequence-specific DNA binding protein with a binding specificity distinct from BF-1 [4].
 

Anatomical context of Foxd1

  • Thus, Foxd1 plays a dual role in the establishment of the binocular visual pathways: first, in specification of the VT retina, acting upstream of proteins directing the ipsilateral pathway; and second, in the patterning of the developing ventral diencephalon where the optic chiasm forms [3].
  • The winged helix transcription factor Foxd1 (previously known as BF-2, Brain Factor 2) is expressed in VT retina, as well as in the ventral diencephalon during the formation of the optic chiasm [3].
  • In fact, the c-kit-positive domain is continuous with a central mesodermal cell mass ventral and lateral to the dorsal aorta, while Foxd1-expressing stromal cells are continuous with a dorsal perisomitic cell population suggesting distinct intraembryonic origins for these cell types [5].
  • Furthermore, they suggest that BF-2 controls the production, by the stroma, of signals or factors that are required for the normal transition of induced mesenchyme into tubular epithelium and full growth and branching of the collecting system [1].
  • Expression of the forkhead/winged helix transcription factor FoxD1 (BF-2) is restricted to stromal cells in the embryonic renal cortex, but it mediates its effects on the adjacent ureteric bud and metanephric mesenchyme, which fail to grow and differentiate in BF-2 null mice [6].
 

Other interactions of Foxd1

  • The BF-1/BF-2 boundary also extends laterally to divide the optic stalk and the retina into nasal (anterior) and temporal (posterior) domains [4].
 

Analytical, diagnostic and therapeutic context of Foxd1

  • In retina-chiasm co-cultures, VT RGCs from Foxd1 deficient retina are not repulsed by chiasm cells, and in vivo many VT RGCs aberrantly project contralaterally [3].

References

  1. Essential role of stromal mesenchyme in kidney morphogenesis revealed by targeted disruption of Winged Helix transcription factor BF-2. Hatini, V., Huh, S.O., Herzlinger, D., Soares, V.C., Lai, E. Genes Dev. (1996) [Pubmed]
  2. Foxd1-dependent signals control cellularity in the renal capsule, a structure required for normal renal development. Levinson, R.S., Batourina, E., Choi, C., Vorontchikhina, M., Kitajewski, J., Mendelsohn, C.L. Development (2005) [Pubmed]
  3. Foxd1 is required for proper formation of the optic chiasm. Herrera, E., Marcus, R., Li, S., Williams, S.E., Erskine, L., Lai, E., Mason, C. Development (2004) [Pubmed]
  4. Expression of winged helix genes, BF-1 and BF-2, define adjacent domains within the developing forebrain and retina. Hatini, V., Tao, W., Lai, E. J. Neurobiol. (1994) [Pubmed]
  5. c-kit delineates a distinct domain of progenitors in the developing kidney. Schmidt-Ott, K.M., Chen, X., Paragas, N., Levinson, R.S., Mendelsohn, C.L., Barasch, J. Dev. Biol. (2006) [Pubmed]
  6. Transcriptional activation of placental growth factor by the forkhead/winged helix transcription factor FoxD1. Zhang, H., Palmer, R., Gao, X., Kreidberg, J., Gerald, W., Hsiao, L., Jensen, R.V., Gullans, S.R., Haber, D.A. Curr. Biol. (2003) [Pubmed]
 
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