The Molecular Mechanism Of Cell Cycle Switch Protein ZmCCS52B Regulating Biomass Accumulation Of Maize

In China, Maize is the first one crop. Increasing its yield is meaningful to solvethe problem of food, energy and resources. The way to increase Maize yield is mainlyby increasing the planting density per unit area. Modifying Maize plant-type andcultivating ideotype is helpful to increase planting density and efficiency. Thus, toclarify the molecular mechanism of Maize’s biomass accmulation and cultivateideotype can help increase the yield per unit area, which possesses great theoreticaland practical significance.Mutants obstained by EMS mutation are important resources to study genesfunction. The traditional ways to clone genes are TILLING and Mapping. These twoways both are low throughput, tiring and expensive. Mutmap is a new way to clonegenes with the help of NGS(Next Generation Sequencing), which is first used in rice.However, the genome of Maize is huge and complicated. It is expensive and difficultto clone genes from Maize using Mutmap. EcMutmap (Exon capture based Mutmap),combining exons capture and Mutmap, is faster, cheaper and less tiring than Mutmap.In our research, we find a mutant with low height, thin stalk, short leaves andears. Using EcMutmap，we successfully map the mutant to its corresponding mutationgene ZmCCS52B and name the mutant zmccs52b-1. In plant, CCS52B, one of theactivator of APC/C complex, regulates the process of cell cycle by choosingsubstrates of APC/C complex. We have made careful observation of phenotypicchanges caused by ZmCCS52B mutation and found that mutation of ZmCCS52B leadsto organ becoming small. But it makes no difference in epidermal cell size andnumber of cells per unit between the mutant and the wild type. Also, we find proteinZmCCS52B is mainly located in cell nucleus. Thus, ZmCCS52B may control the sizeof organs by regulating cell cycle. We have screened proteins that have interactions with ZmCCS52B and found11proteins that may be the substrates of APC/CZmCCS52Bcomplex. Of which,ZmWEE1, one of protein kinases, can restrain the activity of CDK. There may exist2different ways by which ZmCCS52B interact with ZmWEE1to regulate the processof cell cycle. One is that APC/CZmCCS52Bcomplex degrades ZmWEE1. Themutation of ZmCCS52B causes accumulation of ZmWEE1, which restrain theactivity of CDK. The result is cell cycles can not proceed properly. The other is thatZmCCS52B is phosphorylated by ZmWEE1and activates the activity of CDK, whichensures the normal cell cycle. The mutation of ZmCCS52B down regulate the activityof CDK, causing an abnormal cell cycle. However, the way in which ZmCCS52Binteract with ZmWEE1to regulate cell cycle is still unknown.In this article, we use EcMutmap to map mutatant zmccs52b-1to its mutationgene ZmCCS52B rapidly and make an observation of phenotype changes. Yeast twohybrid helps us find11proteins that may have interactions with ZmCCS52B, whichmay be substrates of APC/CZmCCS52Bcomplex. All of this is helpful to uncover themechanism of ZmCCS52B controlling the size of organs and makes it possible tostudy the function of ZmCCS52B and the pathway to regulate cell cycle in whichZmCCS52B involved in.