Reduced RG- II pectin dimerization disrupts differentialgrowth by attenuating hormonal regulation

dc.contributor.authorJewaria, Pawan Kumar
dc.contributor.authorAryal, Bibek
dc.contributor.authorBegum, Rifat Ara
dc.contributor.authorWang, Yaowei
dc.contributor.authorSancho-Andrés, Gloria
dc.contributor.authorBaba, Abu Imran
dc.contributor.authorYu, Meng
dc.contributor.authorLi, Xiaojuan
dc.contributor.authorLin, Jinxing
dc.contributor.authorFry, Stephen C.
dc.contributor.authorVerger, Stephane
dc.contributor.authorRussinova, Eugenia
dc.contributor.authorJonsson, Kristoffer
dc.contributor.authorBhalerao, Rishikesh P.
dc.date.accessioned2025-02-13T07:19:39Z
dc.date.available2025-02-13T07:19:39Z
dc.date.issued2025
dc.descriptionAccepted date: 10 January 2025en_US
dc.description.abstractDefects in cell wall integrity (CWI) profoundly affect plant growth, although, underlying mechanisms are not well understood. We show that in Arabidopsis mur1 mutant, CWI defects from compromising dimerization of RG-II pectin, a key component of cell wall, attenuate the expression of auxin response factors ARF7-ARF19. As a result, polar auxin transport components are misexpressed, disrupting auxin response asymmetry, leading to defective apical hook development. Accordingly, mur1 hook defects are suppressed by enhancing ARF7 expression. In addition, expression of brassinosteroid biosynthesis genes is down-regulated in mur1 mutant, and supplementing brassinosteroid or enhancing brassinosteroid signaling suppresses mur1 hook defects. Intriguingly, brassinosteroid enhances RG-II dimerization, showing hormonal feedback to the cell wall. Our results thus reveal a previously unrecognized link between cell wall defects from reduced RG-II dimerization and growth regulation mediated via modulation of auxin-brassinosteroid pathways in early seedling development.en_US
dc.description.sponsorshipthe work was supported by postdoctoral fellowship from Beijing Advancedinnovation center for tree Breeding by Molecular design, Beijing Forestry University, Beijing,10083, china (P.K.J.). this work was funded by grants vR (vR2020- 03522) and Knut and AliceWallenberg Foundation (KAW 2014- 0032) (R.P.B.); Research Foundation-Flanders (G002121n)(e.R.); the chinese Scholarship council (predoctoral fellowships) (Y.W.); commonwealthScholarship commission for the award of a Ph.d. Scholarship (BdcS-2016-64) (R.A.B.);Bio4eneRGY, Wallenberg Foundation (KAW 2016.0341 and KAW 2016.0352); vinnOvA(2016-00504); and novo nordisk Foundation (nnF21Oc0067282) (S.v.). Author contributions:conceptualization: P.K.J., e.R., and R.P.B. Methodology: P.K.J., S.c.F., B.A., K.J., Y.W., and R.P.B.validation: S.c.F., P.K.J., R.A.B., B.A., and R.P.B. Formal analysis: S.c.F., P.K.J., K.J., B.A., and R.P.B.investigation: P.K.J., S.c.F., R.A.B., G.S.-A., B.A., K.J., A.i.B., Y.W., and M.Y. Resources: S.c.F., R.A.B.,B.A., P.K.J., e.R., J.l., X.l., and R.P.B. data curation: Y.W., P.K.J., and R.P.B. Writing–original draft:P.K.J. and R.P.B. Writing–review and editing: S.v., S.c.F., R.A.B., B.A., M.Y., P.K.J., e.R., J.l., X.l., andR.P.B. visualization: P.K.J., B.A., and K.J. Supervision: S.v., S.c.F., e.R., J.l., X.l., and R.P.B. Projectadministration: R.P.B. Funding acquisition: S.v., R.A.B., Y.W., P.K.J., e.R., and R.P.B.en_US
dc.identifier.citationScience Advances, 11(7): eads0760en_US
dc.identifier.issn2375-2548
dc.identifier.otherdoi/10.1126/sciadv.ads0760
dc.identifier.urihttps://www.science.org/doi/10.1126/sciadv.ads0760
dc.identifier.urihttps://ndkr-library.nipgr.ac.in/handle/123456789/1691
dc.language.isoen_USen_US
dc.publisherAmerican Association for the Advancement of Scienceen_US
dc.subjecthormonal regulationen_US
dc.subjectRG- II pectin dimerizationen_US
dc.subjectdifferential growthen_US
dc.titleReduced RG- II pectin dimerization disrupts differentialgrowth by attenuating hormonal regulationen_US
dc.typeArticleen_US

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