A Maize Kernel Mutant that Lacks a Putative Function in Cell Division

We have identified a new defective kernel (dek) mutant in maize called dek34-Dsg1 with apparent abnormalities in cell division and differentiation. The mutation is caused by an insertion of a GFP-tagged Ds transposable element (DsG) in a gene that is predicted to encode Tel2 Interacting Protein 2 (TTI2). TTI2 is a member of the triple-T (TTT) complex that regulates the maturation and stability of the phosphatidylinositol 3-kinase-related protein kinase (PIKK) family. Early cell divisions during embryo development seem to proceed normally, but eventually arrests at the transition/dermatogen stage. The endosperm is also severely underdeveloped, has highly reduced protein, and lacks histologically distinct compartments. These phenotypes are consistent with mutation in the PIKK member Target of Rapamycin (TOR), which is a major regulator of cell growth and division in response to nutrients. Furthermore, segregation analyses from selfed and reciprocal crosses did not indicate any gametophytic maternal effect, but showed reduced pollen transmission which is consistent with a previously characterized Ataxia Telangiectasia Mutated (ATM) mutant in Arabidopsis, another PIKK member that is involved in DNA damage repair. Taken together, these results show strong evidence for the role of dek34-Dsg1 in PIKK function.