The Recessive Epigenetic swellmap Mutation Affects the Expression of Two Step II Splicing Factors Required for the Transcription of the Cell Proliferation Gene STRUWWELPETER and for the Timing of Cell Cycle Arrest in the Arabidopsis Leaf

Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Conecticut 06520-8104, USA.
The Plant Cell (Impact Factor: 9.34). 08/2005; 17(7):1994-2008. DOI: 10.1105/tpc.105.032771
Source: PubMed


Generally, cell division can be uncoupled from multicellular development, but more recent evidence suggests that cell cycle progression and arrest is coupled to organogenesis and growth. We describe a recessive mutant, swellmap (smp), with reduced organ size and cell number. This defect is partially compensated for by an increase in final cell size. The mutation causes a precocious arrest of cell proliferation in the organ primordium and possibly reduces the rate of cell division there. The mutation proved to be an epigenetic mutation (renamed smp(epi)) that defined a single locus, SMP1, but affected the expression of both SMP1 and a second very similar gene, SMP2. Both genes encode CCHC zinc finger proteins with similarities to step II splicing factors involved in 3' splice site selection. Genetic knockouts demonstrate that the genes are functionally redundant and essential. SMP1 expression is associated with regions of cell proliferation. Overexpression of SMP1 produced an increase in organ cell number and a partial decrease in cell expansion. The smp(epi) mutation does not affect expression of eukaryotic cell cycle regulator genes CYCD3;1 and CDC2A but affects expression of the cell proliferation gene STRUWWELPETER (SWP) whose protein has similarities to Med150/Rgr1-like subunits of the Mediator complex required for transcriptional activation. Introduction of SWP cDNA into smp(epi) plants fully restored them to wild-type, but the expression of both SMP1 and SMP2 were also restored in these lines, suggesting a physical interaction among the three proteins and/or genes. We propose that step II splicing factors and a transcriptional Mediator-like complex are involved in the timing of cell cycle arrest during leaf development.

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    • "Indeed, previously reported regulators for organ size are involved in cell proliferation and expansion (Powell and Lenhard 2012). Some of these factors, such as AINTEGUMENTA (ANT) (Krizek 1999, Mizukami and Fischer 2000), ANGUSTIFOLIA 3 (AN3) (Horiguchi et al. 2005), GROWTH-REGULATING FACTORs (GRFs; Kim et al. 2003), GRFinteracting factors (Kim and Kende 2004), JAGGED (Ohno et al. 2004), STRUWWELPETER (Autran et al. 2002), SWELLMAP 1 (Clay and Nelson 2005), ARGOS (Hu et al. 2003) and KLUH/CYP78A5 (Anastasiou et al. 2007), stimulate cell proliferation during organ development. Overexpression of ANT, ARGOS and KLUH prolongs the period of cell proliferation and consequently increases final organ size without morphological alternation. "
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    • "A number of lines of evidence do indeed indicate that altered cell division pattern does influence leaf shape. For example, mutants in which leaf morphology is altered often display an altered pattern of division termination (Nath et al., 2003), and an extended phase of cell proliferation has frequently been associated with alterations in leaf size and shape (Mizukami and Fischer, 2000; Autran et al., 2002; Clay and Nelson, 2005). Furthermore, experiments in which genes encoding components of the cell cycle have been misexpressed have often led to altered leaf morphology. "
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