Kathleen Newton

Professor of Biological Sciences

PhD, 1980 Indiana University

newtonk@missouri.edu
573-882-4049
324 Tucker Hall

Research description

Although the nucleus contains the vast majority of the genes, mitochondria have their own DNA, coding for proteins vital for the survival of cells. In animals and most plants (including maize), mitochondrial genes are inherited only through the female parent. Plant mitochondrial genomes are generally much larger and more variable than those of animals, and plant mitochondria code for several more proteins than do animal mitochondria. Our laboratory has been leading a project to determine the sequence, organization and gene content of mitochondrial genomes in maize and related grasses.

Mitochondria and chloroplasts have transferred most of the genes necessary for their biogenesis and functioning to the nucleus. This process of organelle DNA transfer to chromosomes is continuing. In collaboration with the Birchler laboratory, we are examining the incorporation of mitochondrial and chloroplast DNA segments into chromosomes of different maize inbred lines and wild relatives of maize.

A long-term project in our laboratory focuses on the generation and consequences of naturally arising mitochondrial mutations in maize. Each of the “nonchromosomal stripe” (NCS) mutations is a deletion resulting from recombination between very small repeats within the mitochondrial genome. Partial deletions of mitochondrial genes that encode specific components of the electron transfer chain complexes or of the mitochondrial translation apparatus, have dramatic effects on plant growth and development. The effects of the mutations can be studied in heteroplasmic plants, which carry some normal mitochondria in addition to the defective organelles. Sorting out of the defective mitochondria during development leads to mutant sectors, allowing us to identify the phenotype associated with each mitochondrial lesion. Mitochondrial mutations have multiple effects within the cell: chloroplast development and photosynthetic function are impacted, resulting in pale stripes. Defective mitochondria also signal to the nucleus of the cell, which then responds to produce a specific set of stress proteins. We are currently attempting to characterize the spectrum of cellular responses to mitochondrial mutations in maize.

Selected publications

Jiao, S.-X., Thornsberry, J., Elthon, T.E. and Newton, K.J. 2005. Biochemical and molecular characterization of Photosystem I deficiency in the NCS6 mitochondrial mutant of maize. Plant Mol. Biol., Vol. 57: 303-313.

Kuzmin, E.V., D.N. Duvick and K.J. Newton. 2005. A mitochondrial mutator system in maize. Plant Physiol. 137:779-789.

Kuzmin, E.V., O.V. Karpova, T.E. Elthon, and K.J. Newton 2004. Mitochondrial respiratory deficiencies signal up-regulation of genes for heat shock proteins. J. Biol. Chem., 279: 20672-20677.

Clifton, S.W., P. Minx, C. M.-R. Fauron, M. Gibson, J. O. Allen, H. Sun, M. Thompson, B. Barbazuk, S. Kanuganti, C. Tayloe, L. Meyer, R. K. Wilson and K. J. Newton. 2004. Sequence and comparative analysis of the maize NB mitochondrial genome. Plant Physiol. 136: 3486-3503.

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