Henry, Susan A.

Cornell Faculty Member

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Professor, Molecular Biology and Genetics (MBG), College of Agriculture and Life Sciences (CALS)

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.

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Northeast Sun Grant Initiative Institute of Excellence

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Biofuels Research Laboratory (BRL)

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David R. Atkinson Center for a Sustainable Future (ACSF) Faculty Fellow

research overview

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).

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GENETIC REGULATION OF PHOSPHOLIPID SYNTHESIS IN YEAST awarded by NATL INST OF HEALTH DHHS 2012 - 2016

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keywords

inositol metabolism
membrane trafficking
phospholipid biosynthesis
signal transduction
transcriptional regulation
yeast genetics

VIVO: Cornell Research & Scholarship

Henry, Susan A.

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