COS 137-7 - The role of invertase isoforms in overcompensation following mammalian herbivory: Are they functionally redundant?

Thursday, August 9, 2012: 10:10 AM
E145, Oregon Convention Center
Madhura H. Siddappaji, Department of Integrative Biology, University of Illinois - Urbana Champaign, Urbana, IL, Steve Clough, Soybean/Maize Germplasm, Pathology, and Genetics Research,, USDA Agricultural Research Service, Urbana, IL, Daniel R. Scholes, Ecology, Evolution and Conserservation Biology, University of Illinois at Urbana-Champaign, Urbana, IL and Ken N. Paige, School of Integrative Biology, University of Illinois - Urbana Champaign, Urbana, IL
Background/Question/Methods

Previous studies have shown that some plants can increase fitness following herbivory by compensating for tissues lost, i.e., they overcompensate.  Yet little is known about the genetic mechanisms leading to enhanced growth and reproduction in plant species exhibiting overcompensation.  Our recent studies have uncovered several genes involved in carbohydrate metabolism that appear to be important in fitness compensation and in particular the phenomenon of overcompensation.  Among others, genes involved include the cytosolic invertases.  Overall there are 12 genes that code for invertase and all are involved in hydrolyzing sucrose. Here we address the issue of functional redundancy of these isoforms in the compensatory response using a combination of gene expression assays and knockout mutants in an Arabidopsis ecotype that overcompensates (Columbia) and an ecotype that undercompensates (Landsberg erecta) following the removal of apical dominance.  

Results/Conclusions

Results indicated elevated expression levels of all invertase genes in Columbia following clipping and higher relative levels of expression than the undercompensating plant Landsberg erecta following clipping.  Although there appears to be functional redundancy in the level of expression for each of the 12 isoforms, knockout studies show a mixture of results from no affect from the knockout to altering the compensatory response from overcompensation to equal or under compensation.  Thus, particular isoforms appear to be differentially important in the phenomenon of overcompensation and are not functionally redundant.