We are interested in how cells in a multicellular
organism assume their developmental fates and form distinct
patterns. We have chosen to address this fundamental question
in the context of Arabidopsis flower development by focusing
on the regulatory mechanism of the floral homeotic gene AGAMOUS
(AG) . AG is a key regulatory gene for flower
development with at least three functions: the specification
of carpel and stamen identity, the repression of sepal and
petal identity, and the control of floral meristem determinacy.
Previous studies established that the activity of AG
is mainly regulated at the transcription level. Negative
regulation of AG transcription is crucial in ensuring stage-
and tissue-specific AG mRNA expression and hence proper
floral organ identity and floral organ pattern. However, little
is known about the mechanism underlying AG transcriptional repression.
We have isolated and characterized three key negative
regulators of AG. They are LEUNIG (LUG)
, SEUSS (SEU) and LARSON
(LSN). We showed that the homeotic transformation
in the floral organ identity of lug
and seu mutants was mediated by precocious and ectopic
AG expression (Liu and Meyerowitz, 1995; Franks
et al., 2002). Further, using a map-based approach,
we have isolated LUG and SEU.
LUG encodes a putative transcriptional
co-repressor with sequence similarity to a class of
transcription co-repressors including Tup1 from
yeast, Groucho from Drosophila, and TLE from mammals
(Conner and Liu, 2000). SEU encodes a novel
protein with at least two glutamine-rich domains
and a conserved domain that shares sequence identity with the
dimerization domain of the LIM-domain-binding transcription
co-regulators in animals (Franks et al., 2002). We
are actively testing the hypothesis that LUG
and SEU may form a co-repressor complex, that is recruited
to the AG cis-regulatory element by other DNA-binding
transcription factors that bind to AG cis-regulatory
elements.
LSN appears to encode an excellent candidate DNA-binding partner of the LUG/SEU co-repressor. lsn mutations enhance the defects of lug , and LSN encodes a putative transcription factor with a DNA-binding motif (Xiaozhong Bao and Zhongchi Liu, unpublished result). Further molecular analyses of how LSN, LUG and SEU interact will provide important insights into the repression mechanism of floral homeotic geneexpression.
in situ hybridization showing AG expression
in a wild-type inflorescence.
AG expression in seu-1 lug-1 double mutant
inflorescence.
A second emphasis in the lab was
the genetic and molecular characterization
of tso1 and tso2 mutants. We are
interested in understanding how inflorescence and floral
meristems are organized and what genes regulate the cell division
activity and cell division orientation in inflorescence
and floral meristems. Mutations in TSO1 cause
defects in cell division in Arabidopsis floral
meristems and cause inflorescence meristem fasciation. We
have isolated the TSO1 gene using the map-based
approach and showed that TSO1 encodes two putative
DNA-binding cysteine-rich repeats and is localized
to the nucleus (Song et al., 2000). Thus,
TSO1 likely encodes a transcriptional factor
that regulates the expression of genes involved in cell division
and meristem organization. Our lab is further characterizing
the TSO1 protein, its localization, and the regulation
of its expression. We have a postdoctoral position open for
this project. If interested, please contact Dr. Zhongchi Liu
via email ( ZL17@umail.umd.edu
).
How are the genes named?
LEUNIG was named after the famous Australian catoonist Michael Leunig because of the resemblance of the horn-like protrutions at the tip of leunig mutant gynoecium to the horn-like protruions in Michael Leunig's cartoon characters. Dr. David Smyth was responsible for naming the gene.
SEUSS and LARSON were both initially identified by mutations that enhance leunig, we decided to name them following the tradition of naming after cartoonist. Bob Franks (a former postdoctoral fellow in the lab) decided to name the two genes after the American cartoonists Dr. SEUSS and Gary Larson.
TSO1 and TSO2 genes are named so because of the ugly floral morphology in tso1 and tso2 mutants. TSO means ugly in Chinese.
Franks, R.G. and Liu, Z. (2001) Floral homeotic gene regulation. Horticultural Reviews vol. 27, 41-77.
Song J, Leung T, Ehler LK, Wang C, Liu Z. (2000) Regulation of meristem organization and cell division by TSO1 , an Arabidopsis gene with cysteine-rich repeats. DEVELOPMENT 127:2207-2217. ( pdf/fulltext )
Liu, Z., Franks, R.G. and Klink, V. P. (2000) Regulation of marginal tissue formation by LEUNIG and AINTEGUMENTA . PLANT CELL 12, 1893-1902. (with Cover ).
Conner, J. and Liu Z. (2000) LEUNIG , a putative transcriptional co-repressor that regulates AGAMOUS expression during flower development. PNAS 97, 12902-12907. (click here to download the pdf file) .
Scovel, G., Altshuler, T., Liu, Z., and Vainstein, A. (2000) The EVERGREEN gene is essential for flower initiation in carnation. J. of Heredity 91, 487-491.
Liu, Z., Running, M. R., and Meyerowitz, E. M. (1997) TSO1 function in cell division during Arabidopsis flower development, DEVELOPMENT 124: 665-672. ( pdf/fulltext )
Liu, Z., and Meyerowitz E. M. (1995). LEUNIG regulates AGAMOUS expression in Arabidopsis flowers. DEVELOPMENT 121: 975-991.