THE DOMINANT DEVELOPMENTAL MUTANTS OF TOMATO, MOUSE-EAR AND CURL, AREASSOCIATED WITH DISTINCT MODES OF ABNORMAL TRANSCRIPTIONAL REGULATIONOF A KNOTTED GENE

The Curl (Cu) and Mouse-ear (Me) mutations of tomato cause two seeming ly unrelated developmental syndromes with a wide range of pleiotropic phenotypes, Yet, the distinct morphogenic alterations in shoots, leave s, and inflorescences conferred by the two mutations appear to be caus ed by unchecked meristematic activity that characterizes dominant muta tions in Knotted1 (Kn1)-like genes of monocot plants, We have been una ble to separate the two closely linked Cu and Me mutations, and they m ay lie in the same gene. A homeobox-containing class I Kn1-like gene, TKn2, also maps to the same location. Significantly, the dominant muta tions are associated with two aberrant modes of TKn2 transcription, Ov erexpression of the two in-frame wild-type transcripts of TKn2 is asso ciated with the Cu mutation, whereas misexpression of an abundant and oversized fusion mRNA is associated with the Me mutation, Available mo lecular evidence strongly suggests that the defective Me-TKn2 transcri pt is generated via a novel splicing event that merges transcripts of two closely linked genes, The translated fusion product is comprised o f most of the 5' end of the adjacent PPi-dependent fructose 6-phosphat e phosphotransferase (PFP) transcript spliced in-frame to coding posit ion 64 of the TKn2 transcript, leaving the TKn2 homeobox intact, We su ggest that class I Kn1-like genes were selected early during evolution to regulate basic programs of aerial meristems and that subtle altera tions in their function may be the basis for the wide diversity in gro wth parameters of shoot systems, leaves, and inflorescences among plan t species.