Dr. Michael Muszynski received his B.A. in Biology in 1985 at the University of Toledo in Ohio and his Ph.D. in Genetics in 1992 from Iowa State University. In 1991, while a graduate student, he was a visiting Ph.D. Student Researcher in the laboratory of Dr. Alfons Gierl at the Max-Planck Institut für Züchtungsforschung in Germany. After a postdoctoral period at the University of Missouri-Columbia, he was a Senior Research Associate then a Research Scientist at Pioneer Hi-Bred International from 1995 to 2007. From 2006 to 2007 he was a Trait Genetics Scientist for Syngenta Seeds. Since 2007, he has been an adjunct assistant professor in the Department of Genetics, Development and Cell Biology here at Iowa State University. Since joining GDCB, Dr. Muszynski has been involved in the teaching of the principles of genetics courses Biology 313 and 313L. In 2013 he was hired as an assistant professor in GDCB.
Plant morphology is determined by the coordinated activity of multiple interacting signaling and regulatory networks. These networks integrate both external and endogenous inputs that help shape final plant form. My overall research goals are to dissect the signaling and regulatory networks which underlie important developmental processes shaping plant morphology and use this information to develop a systems-level understanding of plant growth. My lab uses maize as a model system and combines genetic, genomic, physiological, structure-function and molecular approaches to identify key determinants regulating plant morphology, understand their molecular and biological functions and determine how they interact with other components within larger networks. As network function becomes better defined, our future goals are to use this new knowledge to develop a systems-level understanding of key growth processes.
Ongoing Research Projects
The independent research projects I have ongoing in include functional analysis of determinants controlling (1) maize leaf pattern formation, (2) gametophyte compatibility, (3) the floral transition and (4) inflorescence growth. Below I have summarized some of our results and future directions for each project.
Leaf Pattern Formation.
Maize leaves, like all grass leaves, have a distinct proximal – distal (P-D) growth pattern that is organized along this axis into 4 compartments: the proximal leaf sheath, the auricle, the ligule and the distal leaf blade. This P-D pattern is established early in the developing leaf primordia and proper specification of the four tissues is critical for normal maize leaf development. To elucidate the signaling mechanisms which specify P-D leaf patterning, my lab is studying the semi-dominant Hairy Sheath Frayed1 (Hsf1) mutation, which disrupts normal P-D leaf patterning by causing displacement of proximal tissues into the distal blade. In collaboration with scientists at Dupont/Pioneer Hi-Bred, we cloned the gene responsible for this phenotype and it is Zea mays Histidine-kinase1(ZmHK1), one of the 7 maize histidine kinase (HK) cytokinin receptors. HK cytokinin receptors are part of a two-component signal transduction system that enables cells to respond to cytokinin (CK) and regulate a number of developmental processes. All Hsf1 alleles are missense mutations in the CK-binding domain of ZmHK1 and functional assays indicate inappropriate CK signaling leads to the altered leaf patterning phenotype. Ligand binding and structure-function studies indicate that all the missense mutations localize near the CK binding pocket and alter CK binding affinity. Collectively, these data indicate inappropriate CK signaling alters P-D leaf patterning and suggest normal CK signaling regulates leaf patterning, which is a new function for CKs. Our future studies aim to define the CK signaling network and mechanisms that control leaf patterning. To do this, we are (1) determining transcriptome-wide expression from laser microdissected tissue isolated along different growth axes in normal and Hsf1 mutant leaf primordia using RNA-Seq, (2) characterizing the interaction of ZmHK1 with other CK and auxin signaling proteins in developing normal and Hsf1 mutant leaf primordia using fluorescently tagged proteins and confocal microscopy and (3) making targeted amino acid changes in the CK binding domain and performing functional studies to dissect the mechanism of inappropriate ZmHK1 signaling.
For successful fertilization to occur in maize, the pollen tube carrying the two sperm nuclei must germinate on, penetrate into and grow through the silk (pistil) to reach the ovule. In general, maize is a cross-compatible species, with any variety successfully cross fertilizing any other variety. A dominant allele at the gametophyte factor1 (Ga1) locus prevents cross fertilization with any variety carrying a recessive ga1 allele but only in one direction. Pollen carrying ga1 alleles either do not fertilize or are very inefficient at fertilizing Ga1 silks. Conversely, both Ga1 and ga1 pollen fertilize ga1 silks with equal efficiencies. These results indicate that Ga1 functions gametophytically in the pollen but sporophytically in the silk. Although first described nearly 80 years ago, very little is known about the molecular mechanisms of Ga1 unidirectional cross-incompatibility. To gain insight into the mechanisms underlying Ga1 function and as a first step towards engineering a fertilization-control system in maize, we are using map-based cloning to isolate the Ga1 gene. In collaboration with Syngenta Seeds, we have localized the Ga1 locus to a region of about 170-kb on chromosome 4. We are now collaborating with Paul Scott’s lab (ISU, USDA-ARS) to use numerous approaches to isolate the underlying gene(s). Once isolated, we will confirm the candidate gene through sequence analysis of a number of lines carrying either ga1, Ga1-S (a strong allele) or Ga1-M (an allele with partial function) and by transforming the Ga1-S allele into a ga1 genotype, thereby making it cross incompatible. To uncover the functional properties of the three types of Ga1 proteins we plan to make differentially fluorescent-tagged versions of each – ga1, Ga1-S and Ga1-M – to study their localization and interactions during compatible and incompatible fertilizations.
The Floral Transition
The switch from vegetative to reproductive growth is a critical transition in a plant’s life cycle and has a major impact on plant form. In previous work, I have isolated a number of components and determined their roles within the emerging floral transition network in maize. My lab is continuing this research by isolating a number of additional floral transition mutations affecting both floral activation and repression and working to clone the underlying loci. Our best progress has been with a mutation named fails to transition (Ftt), which is semi-dominant and when homozygous prevents plants from ever flowering. Homozygous Ftt mutant plants never transition and thus grow indefinitely in a vegetative state. The Ftt gene was cloned and it encodes a protein known to be involved in the epigenetic modification of chromatin in other eukaryotes but has not been shown to control flowering in other plant species. To further understand the function of this protein my lab is working to isolate null and weak mutations in this gene. Additionally, we are characterizing transcriptome-wide changes in key tissues important for the floral transition using RNA-Seq and plan to use ChIP-Seq to uncover direct targets of the Ftt protein. Analyses of this and other flowering mutants will allow my lab to further elaborate the maize floral transition network.
Morphology of the inflorescence or floral-bearing structure depends upon the coordination between different growth promoting and growth inhibiting signals that determines final inflorescence shape, size and the number of floral organs formed. Inflorescence growth is a primary determinant of grain yield and is sensitive to numerous stresses, such as temperature and water deficit. In order to identify the molecular determinants regulating inflorescence growth, I have isolated more than a dozen mutations that specifically limit inflorescence growth but have little or no effect on vegetative growth. Phenotypic characterization of these mutants indicates each mutation appears to limit inflorescence growth through different mechanisms, suggesting there are multiple, distinct pathways regulating inflorescence growth. Thus, this collection of mutations offers a rich source of material to define and dissect the networks regulating inflorescence growth. The genes underlying two of these mutations– short ear1 (she1) and truncated inflorescence development1 (tid) – have been cloned. Interestingly, both she1 and tid1 encode proteins involved in the transport of different micronutrients. This was surprising as the transport or accumulation of either of these elements was not previously known to be involved in inflorescence growth. The tid1 gene was cloned independently by Andrea Galavotti (Rutgers University), which he named rotten ear1 (rte1) and we are collaborating on its analysis. Elemental profiling of normal and mutant tissue indicates the accumulation of a number of elements is perturbed in each mutant. We are planning to use a combination of genetic, genomic and physiological approaches to understand how micronutrients function to regulate inflorescence growth.
2156 Molecular Biology
Ames, IA 50011-3650
1985 – 1992 Ph.D., Genetics, Iowa State University, Ames, IA
1980 – 1985 B.A., Biology, University of Toledo, Toledo, OH
- Muszynski, M.G., Moss-Taylor, L., Chudalayandi, S., Cahill, J., Petefish, A., Sakakibara, H., Krivosheev, D., Lomin, S., Romanov, G., Thamotharan, S., Dam, T., Li, B., Trecker, L. and N. Brugière, Inappropriate cytokinin signaling alters leaf patterning in maize. (in prep).
- Meng, X., Muszynski, M.G., and O. N. Danilveskaya, 2011. The FT-like ZCN8 gene functions as a floral activator and is involved in photoperiod sensitivity in maize. The Plant Cell, 23: 942-960.
- Vollbrecht, E., Duvick, J., Schares, J., Ahern, K., Deewatthanawong, P., Xu, L., Conrad, L., Kikuchi, K., Kubinec, T., Hall, B., Weeks, R., Unger-Wallace, E., Muszynski, M., Brendel, V. and T. P. Brutnell, 2010. Genome-wide distribution of transposed dissociation elements in maize. The Plant Cell, 22: 1667–1685.
- Ahern, K. R., Deewatthanawong, P., Schares, J., Muszynski, M., Weeks, R., Vollbrecht, E., Duvick, J., Brendel, V. P. and T. P. Brutnell, 2009. Regional mutagenesis using Dissociation in maize. Methods 49(3): 248-254.
- Borras, L., Zinselmeier, C., Senior, M. L., Westgate, M. E. and M. G. Muszynski, 2009. Characterization of grain-filling patterns in diverse maize germplasm. Crop Science, 49: 999-1009.
- Danilveskaya, O.N, Meng, X., Selinger, D.A., Deschamps, S., Hermon, P., Vansant, G., Gupta, R., Ananiev, E.V. and M.G. Muszynski, 2008. Involvement of the MADS-box gene ZMM4 in floral induction and inflorescence development in maize. Plant Physiology 147: 2054-2069.
- Muszynski, M.G., Dam, T., Shirbroun, D., Hou, Z., Bruggemann, E., Li, B., Archibald, R., Ananiev, E.V., and O. Danilevskaya, 2006. delayed flowering1 (dlf1) encodes a basic leucine zipper protein that mediates floral inductive signals at the shoot apex in maize. Plant Physiology 142: 1523-1536.
- Braun, D.B., Ma, Y., Inada, N., Muszynski, M.G. and R.F. Baker, 2006. tie-dyed1 regulates carbohydrate accumulation in maize leaves. Plant Physiology 142: 1511-1522.
- Ristic, Z., Wilson, K., Nelsen, C., Momcilovic, I., Kobayashi, S., Meeley, R., Muszynski, M., and J. Habben, 2004. A maize mutant with decreased capacity to accumulate chloroplast protein synthesis elongation factor (EF-Tu) displays reduced tolerance to heat stress. Plant Science 167: 1367-1374.
- Danilevskaya O.N., Hermon P, Hantke S, Muszynski M.G., Kollipara K, and E.V. Ananiev, 2003. Duplicated fie genes in maize: expression pattern and imprinting suggest distinct functions. Plant Cell, 15: 425-38.
- Chuck, G., Muszynski, M., Kellogg, E., Hake, S. and R.J. Schmidt, 2002. The control of spikelet meristem identity by the branched silkless1 gene in maize. Science, 298: 1238-1241.
- Papa, C.M., Springer, N.M., Muszynski, M.G., Meeley, R. and S.M. Kaeppler, 2001. Maize chromomethylase Zea methyltransferase2 is required for CpNpG methylation. Plant Cell, 13: 1919-1928.
- Lawrence, C.J., Malmberg, R.L., Muszynski M.G., and R.K. Dawe, 2001. Maximum likelihood methods reveal conservation of function among closely related kinesin families. J. Molecular Evolution , 54: 42 –53.
- Broz, A.K., Thelen, J.J., Muszynski, M.G., Miernyk, J.A. and D.D. Randall, 2001. ZMPP2, a novel type-2C protein phosphatase from maize. J Exp Bot, 52: 1739-1740.
- van Nocker, S., Muszynski, M.G., Briggs, K., and R. M. Amasino, 2000. Characterization of a gene from Zea mays related to the Arabidopsis flowering-time gene LUMINIDEPENDENS. Plant Molecular Biology, 44 (1):107-122.
- Hoekenga, O.A., Muszynski, M.G. and K.C. Cone, 2000. Developmental patterns of chromatin structure and DNA methylation responsible for epigenetic expression of a maize regulatory gene. Genetics, 155: 1889-1902.
- Cao, X, Springer, N.M., Muszynski M.G., Phillips, R.L., Kaeppler, S. and S.E. Jacobsen, 2000. Conserved plant genes with similarity to mammalian de novo DNA methyltransferases. PNAS, 97: 4979-4984.
- Thelen, J.A., Muszynski, M.G., David, N.R., Luethy, M.H., Elthon, T.E., Miernyk, J.A., and D.D. Randall, 1999. The dihydrolipoamide S-acetyltransferase subunit of the mitochondrial pyruvate dehydrogenase complex from maize contains a single lipoyl domain. J Biol Chem, 274: 21769-21775.
- Dawe, R.K., Reed, L.M., Yu, H.-G., Muszynski, M.G., and E.N. Hiatt, 1999. A maize homolog of mammalian CENPC is a constitutive component of the inner kinetochore. The Plant Cell, 11: 1227-1238.
- Yu, H.-G., Muszynski, M.G., and R.K. Dawe, 1999. The maize homologue of the cell cycle checkpoint protein MAD2 reveals kinetochore substructure and contrasting mitotic and meiotic localization patterns. J Cell Biol, 145: 425-435.
- Thelen, J.A., Muszynski, M.G., Miernyk, J.A. and D.D. Randall, 1998. Molecular analysis of two pyruvate dehydrogenase kinases from maize. J Biol Chem, 273: 26618-26623.
- Muszynski, M.G., Gierl, A. and P.A. Peterson, 1992. Genetic and molecular analysis of a three-component transposable-element system in maize. Mol. Gen. Genet. 237:105-112.
- Muszynski, M. G. and M. D. Yandeau-Nelson, 2012. Molecular Genetics of Bioenergy Traits, In C. Kole (ed), Corn Bioenergy Book. CRC Press (in press).
- Danilevskaya, O.N., Meng, X., McGonigle, B. and M.G. Muszynski. (2011). Beyond flowering time: Pleiotropic function of the maize flowering hormone florigen. Plant Signaling & Behavior 6: 1267-1270.
- Goldman, S.L., Sairam, R.V., Muszynski, M.G., Scott, P., Al-Abed, D., and S.D. Potlakayala, 2010. Understanding and manipulation of the flowering network and the perfection of seed quality, In C. Kole, C. Michler, A. Abbott and T.C. Hall (eds), Transgenic Crop Plants, Vol 2: Utilization and Biosafety. Springer-Verlag, 167-198.
- Moose, S.P., Muszynski, MG, Rogowsky, R. and M. Guo, 2009. Putting the function in maize genomics. Plant Gen. 2:103-106.
- Sairam R.V., Al-Abed, D., Johnson, J., Muszynski, M., Raab, M., Reddy, T.V. and S. L. Goldman, 2009. Maize, In: C. Kole and T.C. Hall, (eds), Compendium of Transgenic Crop Plants. John Wiley & Sons, Ltd, 49–82.
- Colasanti, J., and M.G. Muszynski, 2009. The Maize Floral Transition, In S. Hake and J. Bennetzen (eds), Handbook of Maize: Its Biology. Springer Science+Business Media, LLC, 41-56.
Patents and Patent Applications
- Floral transition genes in maize and uses thereof; Danilevskaya, Olga; Auckerman, Milo J.; Hermon, Pedro; Ananiev, Evgueni; Shirbroun, David Mark; Muszynski, Michael G.; issued patent, 7/17/2012; #8222484.
- Delayed Flowering Time (dlf1) gene in maize and uses thereof; Danilevskaya, Olga; Muszynski, Michael G; Li, Bailin; Dam Thao; patent application, November 2007 #20070256198