Analysis of the miR319 target Zmtcptf24 in the maize inflorescence

Abstract

Maize inflorescences are essential for reproduction and also produce seeds that are consumed as food. To understand the genetics pathways that control normal inflorescence development, we study mutants with abnormal inflorescence development. A major focus of the Thompson laboratory is the maize fuzzy tassel (fzt) mutant, which has severe inflorescence defects. fzt contains a mutation in dicer-like 1 (dcl1), which encodes a key enzyme required for microRNA (miRNA) biogenesis. miRNAs are 20-22-nucleotide long RNAs that repress gene expression by directed RNA cleavage or translational inhibition . In fzt mutants, some miRNAs are dramatically decreased, while others are moderately decreased or unchanged. MiR319 is reduced approximately 8-fold in fzt mutants, and is predicted to target mRNAs that encode TCP transcription factors. We hypothesize that reduced miR319 levels may lead to increased or ectopic expression of TCP target genes and be responsible for a subset of the fzt defects. My project focuses on one miR319 target, Zmtcptf24. I used RNA in situ hybridization to examine expression of Zmtcptf24 in normal tassel primordia. Preliminary experiments indicate that Zmtcptf24 is expressed in the carpal, stamens, and lodicules, suggesting that Zmtcptf24 may play a role in maize floral development.