Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Gene Review:

FHL1 - Fhl1p

Saccharomyces cerevisiae

Kleinschmidt, M., Cherel, I., Martin, D.E., Daniel, J., Hall, D.B., et al.

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High impact information on FHL1

We show that regulation of RP gene transcription via TOR and PKA in yeast involves the Forkhead-like transcription factor FHL1 and the two cofactors IFH1 (a coactivator) and CRF1 (a corepressor) [1].
TOR regulates ribosomal protein gene expression via PKA and the Forkhead transcription factor FHL1 [1].
In turn, Sfp1 influences the nuclear localization of Fhl1 and Ifh1, which bind to RP gene promoters [2].
Loss of functional Fhl1p leads to cells that have only 20% the normal amount of RNA and that synthesize ribosomes at only 5-10% the normal rate [3].
In vitro transcription of a UAS(RAP1) enhancer-driven reporter gene requires both Rap1p and TFIID and is independent of the Fhl1p-Ifh1p coregulator [4].

Biological context of FHL1

Conversely, its overexpression by increased gene dosage partially compensates for the genetic inactivation of Fhl1p [5].
Carboxy-terminal deletions removing the last third of the protein lead to a leaky growth phenotype with impaired rRNA maturation, as in the case of the fhl1 deletion [5].
IFH1 (located on chromosome IV) was isolated as a dosage-dependent suppressor partially correcting the growth defect of the fhl1 deletion [5].
One of these upstream activation sequence elements has an ATGTACGGATGT motif, which has previously been described as a putative binding site for the forkhead-like transcription factor Fhl1p [6].
Two other genes, FHL1 and PEP5, are involved in the control of ribosome formation and vacuole biogenesis, respectively; and five genes, presently having unknown functions, could be new potentially interesting candidates for further studies in relation to yeast replicative aging [7].

Associations of FHL1 with chemical compounds

Deletion of FHL1 reduces CPC2 transcription significantly in presence of glucose, but has no effect when the non-fermentable carbon source ethanol is provided [6].
Increased amounts of the Fhl1p co-regulator Ifh1p induce CPC2 transcription even when ethanol is utilized [6].

Physical interactions of FHL1

Surprisingly, loss of Hmo1 abolishes binding of Fhl1 and Ifh1 to RP promoters but does not significantly affect the level of transcriptional activity [8].

Other interactions of FHL1

Hmo1 binding to RP promoters requires Rap1 and (to a lesser extent) Fhl1, proteins that also associate with RP promoters [8].
Occasionally, multiseptate cells were also produced, indicating the involvement of fhl1 and fkh2 in efficient septum cleavage [9].

References

TOR regulates ribosomal protein gene expression via PKA and the Forkhead transcription factor FHL1. Martin, D.E., Soulard, A., Hall, M.N. Cell (2004)
A dynamic transcriptional network communicates growth potential to ribosome synthesis and critical cell size. Jorgensen, P., Rupes, I., Sharom, J.R., Schneper, L., Broach, J.R., Tyers, M. Genes Dev. (2004)
Central role of Ifh1p-Fhl1p interaction in the synthesis of yeast ribosomal proteins. Rudra, D., Zhao, Y., Warner, J.R. EMBO J. (2005)
Yeast TFIID serves as a coactivator for Rap1p by direct protein-protein interaction. Garbett, K.A., Tripathi, M.K., Cencki, B., Layer, J.H., Weil, P.A. Mol. Cell. Biol. (2007)
The IFH1 gene product interacts with a fork head protein in Saccharomyces cerevisiae. Cherel, I., Thuriaux, P. Yeast (1995)
The yeast CPC2/ASC1 gene is regulated by the transcription factors Fhl1p and Ifh1p. Kleinschmidt, M., Schulz, R., Braus, G.H. Curr. Genet. (2006)
Sir-dependent downregulation of various aging processes. Daniel, J. Mol. Genet. Genomics (2005)
An HMG protein, Hmo1, associates with promoters of many ribosomal protein genes and throughout the rRNA gene locus in Saccharomyces cerevisiae. Hall, D.B., Wade, J.T., Struhl, K. Mol. Cell. Biol. (2006)
Characterisation of two novel fork-head gene homologues of Schizosaccharomyces pombe: their involvement in cell cycle and sexual differentiation. Szilagyi, Z., Batta, G., Enczi, K., Sipiczki, M. Gene (2005)