Map-based Cloning And Functional Analysis Of QMIB1,an Inflorescence Branching Number Regulator In Tomato

Flower production and crop yields are influenced by the inflorescence-branching number.Favorable inflorescence-branching number is one of the crucial targets in tomato breeding.Inflorescence meristem(IM)maintenance and termination in flowers is tightly controlled by complex genetic regulatory networks to control the formation of inflorescence branching in tomato.Therefore,identification of genes and exploration of regulatory mechanisms underlying tomato inflorescence branching are very important and have been research highlight.In our work,we identify the QTL,q MIB1(QTL for multiple inflorescence branch 1)to control tomato inflorescence-branching number,which encodes SISTER OF TM3(STM3),a homolog of Arabidopsis thaliana SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1(SOC1).High expression levels of STM3 underlie the highly inflorescence-branching phenotype in ST024 for increase of copies of STM3.STM3 is expressed in both vegetative and reproductive meristematic tissues and in leaf primordia and leaves,indicative of its function in inflorescence-branching development and flowering time.Ch IP-seq and RNA-seq analysis shows STM3 directly binds in the promoter region of FUL1 to activate its expression.Mutation of FUL1 could partially restore inflorescence-branching phenotypes caused by high expression of STM3 in ST024.In addition,STM3 and J2 could form a heterodimer by Y2 H and Co-IP.We characterized the effects of STM3 and J2 as a heterodimer on inflorescence branching using DNA-binding occupancy.We found STM3 and J2 bind on numerous common targets to antagonistically control their expressions.The targets of the STM3-J2 complex include a higher proportion of genes regulating meristem maintenance,such as FUL1,which is a downstream gene that controls inflorescence branching.STM3 and J2 compete aggressively for the same DNA-binding sites: disruption of J2 causes more STM3 binding on their common targets and verse visa that demonstrate their competition for binding common targets.In addition,J2 could bind in the STM3 promoter and repress its expression,revealing the existence of negative feedback regulation in inflorescence branching.Furthermore,J2 mutation can enhance the phenotype of inflorescence-branching increase caused by overexpression STM3,and STM3 mutation can enhance the inhibition of inflorescence branching caused by J2.Taken together,our study revealed the function of STM3 and regulatory mechanism of STM3-J2 heterodimer in the regulation of inflorescence branching.These findings provided a basis for understanding the molecular regulation network of inflorescence-branching development,and a theoretical basis for the selection of inflorescence branching in tomato.