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Molecular Mechanism Of Regulating Endoreduplication And Organ Development By SUD3 Gene In Arabidopsis Thaliana

Posted on:2020-01-21Degree:MasterType:Thesis
Country:ChinaCandidate:Y L ZhangFull Text:PDF
GTID:2370330575992637Subject:Developmental Biology
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The size of organs is an important trait in plants and its regulation is also an important developmental biology problem.Organ size depends on the coordination of cell proliferation and cell expansion.Endoreduplication plays an important role in cell growth and differentiation,but the genes involved in the regulatory network combining endoreduplication with cell growth are largely unknown.It has been reported UBIQUITIN-SPECIFIC PROTEASE 14(UBP14)encoded by DA3 interact with ULTRAVIOLET B INSENSITIVE 4(UVI4)to regulate endoreduplication as well as cell and organ growth in Arabidopsis.The da3-1 mutant in Arabidopsis possesses larger cotyledons and flowers with higher nuclear ploidy compared to Col-0.To further study the relationship between endoreduplication levels,organ and seed size,we performed a genetic screen for the modifiers of da3-1.Several suppressors of da3-1(sud)from the ethyl methane sulfonate(EMS)treated M2 populations of da3-1 were isolated.In this study,we select the sud3 and characterize its phenotypes.The sud3-1 mutation was identified by the mutant mapping(MutMap)approach by using a F2 population of a cross between sud3-1 da3-1 and da3-1.SUD3 has a SKIP-SNW domain,identifying it as a SKI interaction protein and an essential component of the splicing complex.SKIP proteins are highly conserved from yeast to humans.SKIP is involved in circadian clock regulation,abiotic tolerance stress and may be involved in the initiation of splicing and transcription.It is reported that SKIP has transcriptional activation activity in yeast.sud3-1 partially represses the phenotype of da3-1,suggesting that SUD3 may function in the common pathway with DA3.Genetic analyses support that SUD3 acts in a common pathway with UBP14 and UVI4 to control endoreduplication.Biochemical studies demonstrate that SUD3 physically interacts with UBP14 and UVI4 in vivo and in vitro.Our findings reveal an important genetic and molecular mechanism by which SUD3/AtSKIP associates with endocycle regulators UBP14 and UVI4 to modulate endoreduplication and organ growth.By using genetic,biochemical and molecular biology techniques as well as bioinformatics analysis,we explored the regulation of SUD3 gene on endoreduplication and organ development,and provided insights into its possible mechanism of action.
Keywords/Search Tags:Endoreduplication, Suppressor, SUD3, DA3, UVI4
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