Caroline Susan Hill - Selected publications#

Germain, S., Howell, M., Esslemont, G.M., and Hill, C.S. (2000). Homeodomain and winged-helix transcription factors recruit activated Smads to distinct promoter elements via a common Smad interaction motif. Genes Dev 14, 435-451.
This work established the concept that cell type specific responses to TGF-β superfamily members were dictated by expression of specific Smad-interacting transcription factors that recruit activated Smad complexes to DNA. Cited 184 times.

Inman, G.J., Nicolas, F.J., and Hill, C.S. (2002). Nucleocytoplasmic shuttling of Smads 2, 3, and 4 permits sensing of TGF-β receptor activity. Mol Cell 10, 283-294.
(Highlight published in Nature Rev Mol Cell Biol. Oct 2002 p.729. Two-way Traffic).
This work explained how at all times, the concentration of active Smads in the nucleus is directly dictated by the levels of activated receptors. Cited 207 times.

Ross, S., Cheung, E., Petrakis, T.G., Howell, M., Kraus, W.L., and Hill, C.S. (2006). Smads orchestrate specific histone modifications and chromatin remodeling to activate transcription. EMBO J 25, 4490-4502.
This paper identified the Smads as a new class of transcription factor that absolutely require chromatin to assemble then basal transcription machinery and activate transcription. Cited 37 times.

Batut, J., Howell, M., and Hill, C.S. (2007). Kinesin-mediated transport of Smad2 is required for signaling in response to TGF-β ligands. Dev Cell 12, 261-274.
(Featured article and news piece was published in J. Cell Biol. 26 Feb 2007. Motoring to a signaling check-up).
This paper was the first demonstration that Smad2 is transported along microtubules using Kinesin-1 as a motor for
activation at the TGF-β/Activin/Nodal receptors. Cited 32 times.

Levy, L., Howell, M., Das, D., Harkin, S., Episkopou, V., and Hill, C.S. (2007). Arkadia activates Smad3/Smad4-dependent transcription by triggering signal-induced SnoN degradation. Mol Cell Biol 27, 6068-6083.
This paper defined Arkadia’s mechanism of action, showing that it is required for ligand-induced degradation of the potent transcriptional inhibitor, SnoN. Cited 70 times.

Schmierer, B., and Hill, C.S. (2007). TGFβ-SMAD signal transduction: molecular specificity and functional flexibility. Nat Rev Mol Cell Biol 8, 970-982.
This review focused on the mechanism of TGF-β superfamily signalling and how signals are quantitatively transduced and how they are sensed and interpreted by the receiving cells. Cited 338 times.

Daly, A.C., Randall, R.A., and Hill, C.S. (2008). Transforming growth factor β-induced Smad1/5 phosphorylation in epithelial cells is mediated by novel receptor complexes and is essential for anchorage-independent growth. Mol Cell Biol 28, 6889-6902.
This was the first description of a novel arm of TGF-β/Smad signalling through activation of Smad1 in non-endothelial cells, and defined the mechanism by which it occurs. Cited 87 times.

Schmierer, B., Tournier, A.L., Bates, P.A., and Hill, C.S. (2008). Mathematical modeling identifies Smad nucleocytoplasmic shuttling as a dynamic signal-interpreting system. Proc Natl Acad Sci U S A 105, 6608-6613.
(Perspective on this article was published in Science Signaling. Shankaran H and Wiley HS. Smad signaling dynamics: insight from a parsimonious model. Sep 9 2008; Vol 1:pe41.)
This paper described the first tightly constrained, parsimonious computational model for the TGF-β/Smad pathway. Cited 62 times.

Wu, M.Y., Ramel, M.-C., Howell, M., and Hill, C.S. (2011). SNW1 is a critical regulator of spatial BMP activity, neural plate border formation, and neural crest specification in vertebrate embryos. PLoS Biol 9, e1000593
(Highlight published in PLoS Biol. 2011 Feb 15;9:e1001018. SNW1 orchestrates BMP signaling in early embryonic patterning.).
This paper identified SNW1 as a new regulator of BMP activity in early vertebrate embryos. As a result it is critical for neural plate border formation and neural crest specification. Cited 8 times.

Agricola, E., Randall, R.A., Gaarenstroom, T., Dupont, S., and Hill, C.S. (2011). Recruitment of TIF1γ to chromatin via its PHD finger-bromodomain activates its ubiquitin ligase and transcriptional repressor activities. Mol Cell 43, 85-96.
This paper defined the mechanism whereby the E3 ubiquitin ligase TIF1γ represses TGF-β superfamily-induced transcription. Cited 28 times.