To identify which of the candidate genes that are really causing the observed phenotypes and thereby affecting the expression of metacaspase 9 further laboratory studies will be needed. For example:

• Study of mutants carrying T-DNA inserts, for example SALK mutants. T-DNA inserts disrupts the expression of the gene of interest. By crossing these mutants with the AtMC9::nGFP reporter line and allowing the resulting plants to self fertilize approximately 18 % of the offspring would carry both the mutation and at least one copy of the GFP construct. Close examination of the GFP pattern in these homozygous mutant plants would reveal which mutants that have a similar metacaspase 9 expression pattern as the mutant lineage in which the candidate gene was identified.
• Further confirmation of the candidate genes would be gained by conducting transformations to reintroduce fully functional forms of the candidate genes into the original mutant lineages to see which genes that can restore the wild type phenotype.

However three candidate genes were more interesting than the others. Abscisic acid is known to affect polyamine biosynthesis and polyamines are believed to repress PCD genes in immature vessels, preventing premature cell death. This could explain the similarities in GFP expression patterns in the two ectopic expressors. Lignification of the secondary cell wall precedes programmed cell death in vessels, coregulation of these two mechanisms could possibly explain the decreased GFP signal in the roots.