Susan Henry

Susan Henry was the Ronald P. Lynch Dean of the College of Agriculture and Life Sciences (CALS) at Cornell from July 1, 2000 until June 30, 2010 when she returned full time to her position of Professor of Molecular Biology and Genetics. Susan Henry conducts research on genetic regulation of lipid metabolism in yeast. Her research is funded by the National Institutes of Health.

Research Focus

The research in Susan Henry’s laboratory focuses on regulation of membrane lipid metabolism in yeast and its coordination with membrane trafficking and signal transduction (Jesch et al., 2006; Gaspar et al., 2006; Gaspar et al., 2008; Nunez et al., 2008; Gaspar et al, 2010; Villa et al, 2010). We have shown that signals arising from lipid metabolism in the endoplasmic reticulum (ER) and plasma membrane influence major transcriptional networks in the cell (Gaspar et al., 2006a; Jesch et al., 2006; Jesch et al., 2005; Loewen et al., 2004,Jesch et al, 2010). This metabolism influences, and is influenced by, several major signal transduction pathways including the unfolded protein response pathway (Chang et al., 2004; Chang et al., 2002) and the protein-kinase (PKC) pathway (Sreenivas et al., 2001, Nunez et al., 2008, Jesch et al.2010) and the glucose response pathway (Shirra et al., 2001).

Our work has focused on the relationship of transcriptional and metabolic responses to the phospholipid precursor, inositol. The transcription patterns of over 700 genes are altered within two hours (equivalent to about one doubling time) following introduction of inositol. Statistical analysis identified at least six distinct expression responses (Jesch et al., 2005, 2006) including repression of phospholipid biosynthetic genes regulated by Opi1p, as well as genes regulated by the UPR pathway and transient induction of lipid remodeling genes regulated by Mga2p. These three categories of genes are known to respond to signals arising in the ER and the kinetics of the changes in their transcript abundance were rapid, occurring within the first 15 to 30 minutes following introduction of inositol. Analysis of changes in lipid metabolism over the same time frame revealed rapid consumption of phosphatidic acid (PA) which was shown to interact with Opi1p and to be required for its retention in the ER (Loewen et al., 2004). Consumption of PA results in translocation of Opi1p to the nucleus and repression of phospholipid biosynthetic genes including INO1.

Cells defective in Protein Kinase C (PKC) signaling proved to be unable to adapt to growth in the absence of inositol. Wild type cells shifted to inositol-free medium activate PKC signaling via the Mpk1p protein kinase and the Rlm1p transcription factor, upregulating a number of Rlm1p target genes. Cells defective in PKC signaling are unable to mount this transcription response to inositol deficiency and also exhibit major changes in lipid metabolism (Nunez et al., 2008). Interruption of inositol sphingolipid synthesis was shown to trigger PKC signaling (Jesch et al, 2010)

Cells defective in endoplasmic reticulum (ER) to Golgi trafficking such as the temperature sensitive sec13-1 mutant were shown to exhibit major changes in lipid metabolism upon shift to their restrictive temperature. Specifically, these cells exhibited a rapid decrease in synthesis of phosphatidylinositol (PI), while PI synthesis in wild type cells increased at higher temperatures. Simultaneously, sec13-1 cells increased synthesis of triacylglycerols (TAG) and other neutral lipids and accumulated lipid droplets upon shift to the restrictive temperature. Sec13-1 cells in which structural genes for the major TAG synthases were deleted exhibited decreases in their restrictive temperatures, indicating that synthesis of TAG under conditions in which ER to Golgi trafficking is impaired is physiologically relevant (Gaspar et al., 2008).

Outreach and Extension Focus

My role as Dean puts me in contact with constituents related to agriculture, community, and government. My activities on behalf of the College and University are varied and continuous and inform actions in the community, as well as policy in government.

Selected Publications

Journal Publications

• Lastovetsky, O. A., Gaspar, M., Mondo, S. J., LaButti, K. M., Sandor, L., Grigoriev, I. ., Henry, S. A., & Pawlowska, T. E. (2016). Lipid metabolic changes in an early divergent fungus govern the establishment of a mutualistic symbiosis with endobacteria. PNAS: Proceedings of the National Academy of Sciences of the United States of America. 113:15102-15107.

Presentations and Activities

• Stress Response Signaling in yeast; Genomic and Lipidomic Insights from the cellular response to Inositol. Lipid Maps Annual Meeting May 13-14 2014. May 2014. Lipid Maps. San Diego.
• The Cellular Response to Inositol: Regulation of Glycerolipid Metabolism and Stress Response Signaling. 5th Lipotox Meeting, Graz, Austria, March 13-14, 2014. March 2014. University of Graz. Graz, Austria.
• Inositol as a Regulator of Metabolism and Stress Response Signaling. International Yeast Lipid Conference. May 2013. IYLC organizing committee. Halifax, Nova Scotia, Canada.
• The Dynamic Roles of Phospholipids and Triacylglycerols in Regulation and Signaling in Yeast. American Society for Biochemistry and Molecular Biology (ASBMB)Annual Meeting . April 2013. ASBMB. Boston.
• Avanti Prize Lecture:The Dynamic Roles of Phospholipid and Triacylglycerol Metabolism in Regulation and Signaling in Yeast in Regulation and Signaling in Yeast. Experimental Biology 2013. April 2013. American Society for Biochemistry and Molecular Biology (ASBMB). Boston.
• The roles of inositol containing phospholipids and sphingolipids in calcineurin and PKC signaling in yeast. 2012 FASEB Science Research Conference on Phospholipid Metabolism: Diesease, Signal Transduction, and Membrane Dynamics. July 2012. Federation of Societies for Experimental Biology (FASEB). Saxtons River ,VT.
• Brushes with Genius, Cornell Faculty members recall Barbara McClintock. Panel Discussion. August 2010. Division of Rare and Manuscripts Collections, Carl A Kroch Library, Cornell University. Ithaca, NY.