UMass Boston

Cell Biology: Signal Transduction and Regulation of Cell Morphology

PhD, Biology, California Institute of Technology

BS, Biology, University of California, Los Angeles, 1988

Education Abroad Program, University of Sussex, England, 1986-87

• Durant M, Mucelli X, Huang LS. (2024) Meiotic Cytokinesis in Saccharomyces cerevisiae: Spores That Just Need Closure. J. Fungi, 10: 132, doi.org/10.3390/jof10020132. (Part of the Special Issue “Yeast Cytokinesis”, edited by Erfei Bi and Jian-Qiu Wu.)
• B.C. Seitz*, X. Mucelli*, M. Majano, Z. Wallis, A.C. Dodge, C. Carmona, M. Durant, S. Maynard, and L.S. Huang (2023) Meiosis II spindle disassembly requires two distinct pathways. Molecular Biology of the Cell. 34: ar98 (* = equal contribution)
• M. Durant*, J.M. Roesner*, X. Mucelli, C.J. Slubowski, E. Klee, B.C. Seitz, Z. Wallis, and L.S. Huang (2021) The Smk1 MAPK and Its Activator, Ssp2, Are Required for Late Prospore Membrane Development in Sporulating Saccharomyces cerevisiae. J. Fungi 7: 53. doi: 10.3390/jof7010053. (Part of the Special Issue “Formation and Function of Fungal Ascospores”, edited by Aaron Neiman.) (* = equal contribution)
• S.M. Paulissen, C.A. Hunt, B.C. Seitz, C.J. Slubowski, Y. Yu, X. Mucelli, D.Truong, Z. Wallis, H.T. Nguyen, S. Newman-Toledo, A.M. Neiman, L.S. Huang (2020). A Non-canonical Hippo Pathway Regulates Spindle Disassembly and Cytokinesis During Meiosis in Saccharomyces cerevisiae. Genetics. 216: 447-462.
• S.M. Paulissen and L.S. Huang (2016) Efficient sporulation of Saccharomyces cerevisiae in a 96 multiwell format. J. Vis. Exp., doi: 10.3791/54584
• S.M. Paulissen, C.J. Slubowski, J.M. Roesner, and L.S. Huang (2016) Timely closure of the prospore membrane requires SPS1 and SPO77 in Saccharomyces cerevisiae. Genetics 203: 1203-1216
• E.M. Parodi, J.M. Roesner, L.S. Huang (2015) SPO73 and SPO71 function cooperatively in prospore membrane elongation during sporulation in Saccharomyces cerevisiae. PLoS One 10: e0143571.
• C.J. Slubowski, A.D. Funk, J.M. Roesner, S.M. Paulissen, and L.S. Huang (2015) Plasmids for C-terminal tagging in Saccharomyces cerevisiae that contain improved GFP proteins, Envy and Ivy. Yeast 32: 379-387.
• C.J. Slubowski, S.M. Paulissen, and L.S. Huang (2014) The GCKIII kinase Sps1 and the 14-3-3 isoforms, Bmh1 and Bmh2, cooperate to ensure proper sporulation in Saccharomyces cerevisiae. PLoS One 9: e113528.
• E.M. Parodi, C.S. Baker, C. Tetzlaff, S. Villahermosa, and L.S. Huang (2012) SPO71 mediates prospore membrane size and maturation in Saccharomyces cerevisiae. Eukaryotic Cell 11: 1191-1200.doi:10.1128/EC.00029-12.
• E.M. Davison, A.M. Saffer, L.S. Huang, J. DeModena, P.W. Sternberg, and H.R. Horvitz (2011) The LIN-15A and LIN56 transcriptional regulators interact to negatively regulate EGF/RAS signaling in Caenorhabditis elegans vulval cell-fate determination. Genetics 187: 803-815.
• L.S. Huang and C. Vaughn (2009) Question Bank for Essential Cell Biology, ed. 3. Garland Sciences (New York).
• K.R. Benjamin and L.S. Huang (2008) Test Questions for Molecular Biology of the Cell, ed 5. Garland Sciences (New York).
• K.L. Auld, A.L. Hitchcock, H.K. Doherty, S. Frietze, L.S. Huang, and P.A. Silver (2006) The conserved ATPase Get3/Arr4 modulates the activity of membrane-associated proteins in Saccharomyces cerevisiae. Genetics, 174: 215:227.
• L.S. Huang and P.W. Sternberg (2006) Genetic dissection of developmental pathways, WormBook, ed. The C. elegans Research Community, doi/10.1895/wormbook.1.88.1, http://www.wormbook.org.
• L.S. Huang, H. K. Doherty, and I. Herskowitz (2005) The Smk1p MAP kinase negatively regulates Gsc2p, a 1, 3-beta-glucan synthase, during spore wall morphogenesis in Saccharomyces cerevisiae. Proc. Natl. Acad. Sci. 102: 12431-12436.
• K.R. Benjamin and L.S. Huang (2004) Testbank for Essential Cell Biology, ed. 2. Garland Sciences (New York).

Research Interests

Linda Huang's research focuses on meiosis, a process which is essential for the creation of gametes, which are sperm and eggs in humans and spores in yeast. The work in her laboratory uses sporulation in the budding yeast, Saccharomyces cerevisiae, as a model to study the regulation meiosis and how the cellular events that occur during gametogenesis are coordinated.

During sporulation, a diploid yeast cell undergoes meiosis and spore formation, to form four haploid spores. These four spores form de novo within the original mother cell, each spore housing one of the four meiotic products. A highly organized four-layered spore wall surrounds each of the four spores. The events of spore morphogenesis control the appropriate formation of these spores. Spore morphogenesis begins with the development of the prospore membrane during meiosis II. The prospore membrane will eventually become the plasma membrane of the newly formed spore. The closure of the prospore membrane at the end of meiosis II is the cellularization event for the spore, and is how cytokinesis occurs in meiosis II during sporulation. Recently, the Huang Lab has been focusing on the process of exit from meiosis II, examining how the regulation of meiosis is coordinated with the cellular events that occur at the end of meiosis II. The Huang Lab uses genetics, cell biology, molecular biology, and biochemistry to study this process.

Work from the Huang Lab has helped define the pathway regulating exit from meiosis II. Specifically, exit from meiosis II utilizes the Sps1 STE20-family GCKIII kinase, acting downstream of the Cdc15 Hippo-like kinase, to coordinate the cellular events of meiotic exit. Interestingly, this is different from the regulation of mitotic exit, where Cdc15 activates the Mob1/Dbf2 NDR/LATS kinase complex instead of Sps1. The Huang lab has demonstrated that the timing of prospore membrane closure requires the Cdc15-Sps1 pathway acting in parallel with Ama1-APC/C. These two pathways also regulate meiosis II spindle disassembly. Current work is focused on understanding the Cdc15-Sps1 pathway: defining how this pathway is activated, defining other components of this pathway, and defining downstream targets used for the cellular changes that occur during exit from meiosis II.