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THE PLANT CELL, Vol 9, Issue 12 2143-2158, Copyright © 1997 by American Society of Plant Biologists
The Dominant Developmental Mutants of Tomato, Mouse-ear and Curl, Are Associated with Distinct Modes of Abnormal Transcriptional Regulation of a Knotted Gene
A. Parnis, O. Cohen, T. Gutfinger, D. Hareven, D. Zamir and E. Lifschitz
Department of Biology, Technion-Israel Institute of Technology, Haifa 32000, Israel
The Curl (Cu) and Mouse-ear (Me) mutations of tomato cause two seemingly
unrelated developmental syndromes with a wide range of pleiotropic
phenotypes. Yet, the distinct morphogenic alterations in shoots, leaves,
and inflorescences conferred by the two mutations appear to be caused by
unchecked meristematic activity that characterizes dominant mutations in
Knotted1 (Kn1)-like genes of monocot plants. We have been unable to
separate the two closely linked Cu and Me mutations, and they may lie in
the same gene. A homeobox-containing class I Kn1-like gene, TKn2, also maps
to the same location. Significantly, the dominant mutations are associated
with two aberrant modes of TKn2 transcription. Overexpression of the two
in-frame wild-type transcripts of TKn2 is associated with the Cu mutation,
whereas misexpression of an abundant and oversized fusion mRNA is
associated with the Me mutation. Available molecular evidence strongly
suggests that the defective Me-TKn2 transcript is generated via a novel
splicing event that merges transcripts of two closely linked genes. The
translated fusion product is comprised of most of the 5[prime] end of the
adjacent PPi-dependent fructose 6-phosphate phosphotransferase (PFP)
transcript spliced in-frame to coding position 64 of the TKn2 transcript,
leaving the TKn2 homeobox intact. We suggest that class I Kn1-like genes
were selected early during evolution to regulate basic programs of aerial
meristems and that subtle alterations in their function may be the basis
for the wide diversity in growth parameters of shoot systems, leaves, and
inflorescences among plant species.
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