Journal of Cell Science utpelyr fcnrladipiain o aging for implications general and in by control regulation of – layers death multiple and senescence leaf Plant Commentary gn,btmsl satgtyrgltdpoeswt crucial a with process regulated tightly a during Leaf tear’ is death. and mostly ‘wear their but of by process aging, followed the involves stage, partly senescence senescence Leaves the become leaf nutrients. enter they as accumulate then growth, life and their and competent initiate development photosynthetically Leaves their energy. they During because light primodia. earth on using food carbon of source fix practical only the cell perhaps further is undergo 2008). for Sedivy, capacity and cells, (Jeyapalan the aging of of upon senescence loss division the mitotic to for the refers used which in mostly and the animals, senescence is in color of senescence whereas 1), term type leaf (Box This senescence in post-mitotic leaves. is plants autumn changes of is spectacular level death their organ subsequent at the the fields at in wheat senescence and plant manifested soybean contrast, The By corn, plant times. 1). entire rice, the harvest most (Fig. in of al., observed level levels levels, at be et death organismal can various and age-dependent (Lim and senescence at plant organ death of the outcome occurs the to biology. plants at leading cells, as distinctively in organism, of in Senescence entire defined process 2007a). the questions degeneration is or fundamental and organs with plants degradation are life programmed in organisms their die living end why Senescence and and age, How they death. senesce by after followed organisms, senescence all Virtually Introduction general. regulation and Post-translational in system- regulation, chromatin aging our Translational for of enable implications to level latest necessary possible words: the the perspectives their Key discusses at the with Commentary including presents together This and senescence, regulation, mechanisms, regulation. leaf of molecular of a post-translational layers underlying is understanding and senescence multiple the level leaf translational into molecular by that to post-transcriptional, insights apparent key evolved controlled now by and the has is tightly that understanding understandings as It in strategy towards is analyses. well a progress ‘omics’ culminate that is as as significant thus well program been transcription, that and as has genetic studies, plant, transitions there molecular the complex the decade, and of during metabolic genetic past highly parts produced using the other are senescence and that or During leaf a nutrients seeds plant. of physiological the developing provide the principles of to of leaves degradation developmental, redistribution assays. fitness the Plant their for experimental the of and allows death? for maximize leaf that accessible series and the death’ readily of ‘altruistic senescence a are an phase towards is and growth undergo senescence age history Leaf life they death. leaves reproducible and when show senescence lifespan, fate they their because their question change this Throughout cells explore and to tissues window unique organs, organisms, do How Summary 10.1242/jcs.109116 doi: 4823–4833 126, ß Science Cell of Journal ( correspondence for *Authors 2 1 Woo Ryun Hye cdm fNwBooyfrPatSnsec n ieHsoy nttt o ai cec,DIT ag 1-7,Rpbi fKorea of Republic 711-873, Daegu DGIST, Science, Korea Basic of for Republic Institute 711-873, History, Daegu Life (DGIST), and Technology Senescence and Plant Science for of Biology Institute New Gyeongbuk of Daegu Academy Biology, New of Department 03 ulse yTeCmayo ilgssLtd Biologists of Company The by Published 2013. h efi h ra htcaatrzspat sattoh and autotrophs as plants characterizes that organ the is leaf The gn,La eecne hoai-eitdrglto,Tasrpinlrglto,Ps-rncitoa regulation, Post-transcriptional regulation, Transcriptional regulation, Chromatin-mediated senescence, Leaf Aging, 1 y ugKim Jung Hyo , [email protected] ; [email protected] 2 ogGlNam Gil Hong , ) 1,2, n yn kLim Ok Pyung and * rgeso n opein(o )(uhnnWlatne al., et onset, (Buchanan-Wollaston its 2) endogenous adjust (Box various to completion to order and and in progression leaf factors the environmental of exogenous stages and respond life that previous pathways the of to regulation comprehensive and intricate plant. crucially a that of survival strategies and developmental fitness the active to are contribute leaves and have senescence in that Thus, death leaves. nutrients autumn of senescing from utilization relocated of the been blooming utilized through The are occurs flowers. or and flowers leaves roots spring new or of development stems the in degraded for are stored later that are nutrients senescence the leaf trees, during In al., to fruits. relocated et and are seeds molecules (Watanabe hydrolyzed developing phase these plants, growth annual the In 2013). during accumulated pigments were and acids that nucleic of lipids, (ROS) hydrolysis proteins, 1988). the as species such include Leshem, macromolecules, senescence 1987; oxygen leaf Lake, during reactive changes and Metabolic (Thompson include in 1C) increase plants (Fig. are generation the which in leakiness, with membrane senescence and associated peroxidation of lipid in leaf symptoms of increases stages the final Other contrast, the until In senescence. intact chlorophylls. remain of nucleus breakdown and the the of mitochondria change to the owing by color accompanied cellular is leaf it of in where observed 1B), distinctively degradation most (Fig. is chloroplasts the this manner; and orderly an metabolism in structures cellular dramatic in a undergo transition cells leaf senescence, During purpose. biological efsnsec rceswt g,bttepoesivle an involves process the but age, with proceeds senescence Leaf 1, * 4823 Journal of Cell Science oeua rnilso efsnsec n et,adhave and key and death, the modes. genetic regulatory and unravel multi-layered extensive of senescence to involvement leaf the undertaken decade, and revealed of been principles productivity past have molecular plant the efforts to the molecular is During genes what and senescence fitness? 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(JA), HDA6 acid flowering many jasmonic and in to senescence response of involved the levels leaf is including global development, the regulates and affects that acetylation HDA6 2008). histone factor al., et well-known (Wu histone senescence another RPD3-type is an (HDA6), deacetylase, 3 DEACETYLASE HISTONE nml,teiprac fmRA nrgltn cellular regulating In known. in well is miRNAs processes important of aging be and importance senescence to In the level. reported post-transcriptional the animals, been at mRNAs RNAs have post-transcriptional control that small-interfering regulators miRNAs, as and undergo such Recently, (siRNAs) stability. 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Drosophila Gere al., et (Greer Arabidopsis .elegans C. n miR- and results , i30pooe efsnsec ycnrligtelvlo the that of suggests level the observation controlling This by TAS3 2010). senescence al., leaf et promotes miR390 Marin 2010; the al., of et triggers class from miR390 is generated plant-specific targets are their example, that a tasiRNAs For the of tasiRNAs, production RNAs. the small are endogenous leaf senescence important leaf Taken animals. as in as 2008). well miRNAs as al., plants, implicate in regulators et reports senescence (Schommer these senescence together, leaf premature age- for comprising 3) senescence (Box leaf pathway dependent feed-forward trifurcate a of postulation the in results of ultimately EIN2, upregulation of activation with by expression the miR164 through regulated this aging, in negatively decrease leaf of gradual is expression The 3). senescence the (Fig. above, leaf miR164 mentioned of As regulator 2009). positive al., et (Kim euaino efsnsec slkl oivleadditional involve to likely the is and senescence thought leaf in previously role of than larger regulation much processes a biological play diverse to appears regulation transcriptional of senescence, overexpression leaf delayed whereas biosynthesis. exhibit JA modulating senescence, plants by and miR319-overexpressing partly growth TCP senescence, leaf the leaf coordinate regulates transcription targets, to appear its which through factors, BRANCHED/CYCLOIDEA/PCF) miR319, miR164, (TEOSINTE to addition In et rcs.Tefgr saatdfo i ta.(i ta. 2009) cell al., et and (Kim between al. et senescence Kim transitions from adapted leaf is of figure age-dependent The process. paradigm death in new networks the pathway, a miR164 regulatory the of demonstrating presence of al., the EIN2 to et thereby of owing induction death because (Kim to transient lead a aging not that does shows upon stages further robust death modeling a The EIN2. ensures is later 2009). loop that by life, trifurcate mechanism their the expression leaf biological that of suggests miR164 at modeling stages of Mathematical earlier its alleviated downregulation and at age-dependent death miR164 is cell by which in EIN2. regulated by role manner negatively age-dependent positive is an in a a induced is has ORE1 is 2009). expression that al., et factor (Kim miR164 transcription and ANAC092) death as factor, cell known transcription also NAC-family age-dependent plant-specific (a for ORE1 EIN2, pathway involves feed-forward trifurcate The death cell age- and for senescence pathway dependent feed-forward Trifurcate 3. 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ARF2 TCP4 . miR164 ,a EIN2 miR319 , ORE1 ORE1 EIN2 SAG12 agt causes target, TAS3 n miR164. and ORE1 n of one ; Journal of Cell Science eea e iae n hshtsshv nipratrl in role important an the protein have is phosphatases phosphatases senescence; and kinases and leaf key implicate of kinases several aging of protein during numerous regulation altered analyses of the expression in expression phosphorylation Genome-wide of phosphorylation level Protein additional below. discussed an as as and senescence, as post- leaf stability that emerging of surprising control is not activity, such is regulation it conformation, translational Therefore, proteins. the of modifications, localization affect and methylation acetylation ubiquitylation, post-translational glycosylation, phosphorylation, Different regulation Post-translational leaf of regulation elucidate translational extensive the to the senescence. undertaken underlie Further of be that level. expression mechanisms to the need translational the approaches the coordinates profiling that protein implying at that species, subunits mechanism mRNA Rubisco two a the is of modulation there rate a translation through tightly for the compensated difference is of the mRNA Interestingly, be of gradually RBCS. amount of in the levels in subunits that mRNA must the than in RBCS slower decline is expression the RBCLs of but aging, levels leaf their during decrease mRNA to holoenzyme, The stoichiometrically gene assembled coordinated. different the be in to encoded As form need are subunits. but RBCL components RBCS the compartments, Rubisco 1989). with the two assembled into al., subunits, are these transported et large and they cytoplasm (Dean where eight is the plastid, genes in of the plants translated plastid by and are subunits higher encoded RBCL genes, are by nuclear in which encoded of subunits, Rubisco family small RBCS 2013). eight senescence leaf of Makino, rice composed during and level translational (Suzuki is the subunits at controlled (Rubisco) carboxylase/oxygenase 1,5-bisphosphate translational senescence. between leaf and relationship genes plastid the provide Syntichaki of might 2007; regulation into PRPS17 al., of insights et characterization important Further Hansen extends 2007). 2005; al., translation al., et mRNA et reduced (Arquier that lifespan shown have and aging, in studies recent Drosophila several Similarly, chloroplast. of expression component reduced a ore4 the is ribosome, PRPS17 plastid Because the 2002). of al., et (Woo phenotypes 17 the PROTEIN of mutation for challenge senescence. important leaf is an underlying be mechanisms little will the role a translational unveiling its the only at elucidating senescence and a However, leaf level, in of scenarios. regulation expression the biological about gene and known of modulate initiation further range to wide translation known is including elongation, regulation, Translational regulation Translational transcripts. antisense natural ncRNAs long alternative and decay, nonsense-mediated including editing, mRNA mechanisms, splicing, post-transcriptional of types 4830 nitrsigrcn td on httesnhsso ribulose of synthesis the that found study recent interesting An The uati xetdt euti eue rnlto aei the in rate translation reduced in result to expected is mutant Arabidopsis ora fCl cec 2 (21) 126 Science Cell of Journal aervae ikbtenpoensnhssand synthesis protein between link a revealed have ( PRPS17 LSI IOOA ML SUBUNIT SMALL RIBOSOMAL PLASTID mutant ee xiisdlydla senescence leaf delayed exhibits gene, ) Arabidopsis ore4 hc osse knockdown a possesses which , Bez ta. 01,and 2011), al., et (Breeze .elegans C. 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GmSARK to of and auxin responses ethylene, altered exhibit ob oiiergltr fla eecne(ue l,01.The al.,2011). et GmSARK-overexpressing (Xu that senescence found leaf of authors regulators positive be leaf to KINASE regulate its and to (GmSARK) RECEPTOR-LIKE targets and ( its SENESCENCE-ASSOCIATED receives Soybean investigation. to RPK1 further requires which 2011).senescence signals al., by senescence mechanism et transduces (Lee exact senescence the leaf However, age-dependent and 2011). induced in al., mutations function Loss-of- senescence. et leaf age-dependent regulatory and ABA-mediated important in an throughrole (Lee has ABA-inducible and an probably kinase is signaling receptor membrane-bound (RPK1) senescence, 1 hormone KINASE PROTEIN leaf RECEPTOR plant of modulating regulators AHK3 important the senescence. ARR2 leaf that which controls suggesting AHK3 not, in by does phosphorylation mutated ARR2 is site of phosphorylation overexpression of Furthermore, senescence, 2006). overexpression al., et whereas (Kim manner cytokinin-dependent a of overexpression B transgenic and AHK3 mutant gain-of-function this hshrlto nterglto fla eecneis senescence leaf of regulation the in stressphosphorylation biotic WRKY53. coordinate through senescence to of appears induction the MEKK1 with (Pitzschke Thus, response established 2009). well al., in also been MEKK1–MKK1/2–MPK4 et have involves signaling is stress that biotic of it cascade roles The pathway; 2007). MAPK al., et MAPK (Miao the to promoters target the ability its its at of DNA increases to which bind target 3), (Fig. a MEKK1 also by phosphorylated is also WRKY53 it although factor transcription senescence, above-mentioned The leaf target(s). additional promote have by might to obtained MPK6 of phenotype upstream of senescence of premature mutation overexpression the loss-of-function suppresses the Notably, mpk6 of overexpression Arabidopsis the and 2009) Arabidopsis al., of et (Zhou expression MPK6 activates directly and MKK9 (MPK6). phosphorylates 6 KINASE MAP and (MKK9) 9 KINASE mitogen- KINASE the MAP cascade, of signaling (MAPK) members kinase protein the activated as such senescence, leaf modulating uaini h xrclua oanof domain extracellular ( remained the mutant long in of a mutation senescence mechanism until plant molecular of unknown the delay However, cytokinin-mediated senescence- potent hormones. are Cytokinins retarding activity. kinase histidine with Arabidopsis Arabidopsis eety w eetrlk rti iae eeietfe as identified were kinases protein receptor-like two Recently, nte neetn xml o h oeo protein of role the for example interesting Another oso-ucinmtn lososdlydla senescence. leaf delayed shows also mutant loss-of-function eae efsnsec Kme l,20) R2 type- a ARR2, 2006). al., et (Kim senescence leaf delayed uatehbt eae efsnsec,whereas senescence, leaf delayed exhibits mutant itdn iae3(H3,actknnreceptor cytokinin a (AHK3), 3 kinase histidine Zo ta. 09.The 2009). al., et (Zhou epnergltr spopoyae yAK in AHK3 by phosphorylated is regulator, response MKK9 MKK9 Arabidopsis MKK9 SARK Arabidopsis RPK1 nrae uigla eecnein senescence leaf during increases ed opeoiu efsnsec.The senescence. leaf precocious to leads niaigta K9functions MKK9 that indicating , ih euaela eecne as senescence, leaf regulate might edt infcn ea nABA- in delay significant a to lead ore12-1 ARR2 ooo ASR)wr shown were (AtSARK) homolog ooo tAKrslsin results AtSARK homolog ihagain-of-function a with ) ed odlydleaf delayed to leads mkk9 AHK3 Arabidopsis MPK6 loss-of-function a isolated; was lcn max Glycine partially plants ) Journal of Cell Science otcssdgae bqiyae agtpoen,decreases proteins, target ubiquitylated in which degrades proteasome, the cases of activity most the physiological In systems, 2012). Rape, diverse animal and various (Komander in stress signaling hormone environmental step and progression, responses being regulatory cycle cell key including is processes, a modification as recognized post-translational Ubiquitin-mediated ubiquitylation Protein ulnFbxpoen(C)E iaecmlx SCF complex, ligase E3 F-box (SKP1)/ (SCF) an 1 is protein protein kinase-associated ORE9 Cullin/F-box S-phase 2011). an al., forms et and (Nelson protein as karrikin Umehara well and 2008; 2008) as al., al., 2002), AXILLARY et et al., (Gomez-Roldan et strigolactone MORE photomorphogenesis (Stirnberg by in branching as signaling 2007), involved al., to also et is referred (Shen (MAX2), also work 2 Subsequent ORE9, GROWTH 2001). al., that et Woo senescence showed 1997; leaf al., delayed et with (Oh mutants phenotypes for screen genetic forward proteasomes. selective 26S subsequent the their responsible by and are degradation Ub-ligases proteins E3 Several of the polyubiquitylation with senescence. plants, for in associated leaf and of are senescence, leaf regulation pathways the degradation for ubiquitin-dependent important to appear be related also proteins to causally ubiquitin-like and be ubiquitin by might modifications (Lo changes diseases age-associated these and aging and aging, during eecnei euae yatgtycnrle eei program address genetic leaf controlled that tightly questions obvious a now by is regulated biological It is processes. senescence many assembly and ordered of biogenesis provides whereas process the senescence investigate degradation, aging, leaf to with opportunity Furthermore, unique associated another death. are and that processes senescence genetic understand amenable readily to and unique system a are leaves plant Evidently, perspectives future and Conclusions reports available suggest. few far might the here is senescence than discussed senescence regulation leaf leaf ubiquitin-mediated for of important that more context anticipate the We within control. and function ubiquitylation molecular for Future targets their senescence. the leaf determining of include control challenges the importance in the ubiquitylation support studies protein these of together, Taken 2012). al., et WRKY53 WRKY53 in involved of activity. phenotype is ubiquitin-ligase senescence its UPL5 The through Here, probably 2010). that most degradation, Zentgraf, implying and WRKY53, (Miao of WRKY53 UPL5, overexpression ligase inducible to ubiquitin-protein E3 binds domain been which HECT has leaf the of degradation for control protein shown the ubiquitin-mediated for evidence by direct senescence more A regulators senescence. negative leaf key of including substrates, specific target might xrsino e eecnergltr,sc as the such addition, regulators, In senescence conditions. key low-light of expression under plant ubiquitin- of regulator senescence E3 negative a as U-box-armadillo is SAUL1 leaf plant senescence, 2009). UBIQUITIN al., a et in (Raab through (SAUL1), ligase SENESCENCE-ASSOCIATED involved 1 of senescence regulator ubiquitin-ligase LIGASE is positive leaf Another a senescence regulates is senescence. which UPL5 WRKY53, supportingleaf of further that degradation WRKY53, the overexpressing notion plants the of that to The rbdpi ore9 Arabidopsis and WRKY6 saul1 satrdin altered is oso-ucinmtnsdslyearly display mutants loss-of-function uatwsoiial sltdfo a from isolated originally was mutant UPL5 UPL5 eut ndcesdlvl of levels decreased in results w 01.Post-translational 2011). ¨w, koku lnsi similar is plants -knockout saul1 uat (Vogelmann mutants ORE9 which , ORE1 , rca etse oad etrudrtnigo leaf maps, as of localization approaches. such these protein into understanding sets, integrated or also data better interactions be could system-level genetic a a Other and be towards protein death. will and step modeling, senescence computational next with multiple crucial coupled RNA at total points, phenome of the and time use of metabolome the analysis proteome, regard, as transcriptome, this such that In approaches, process in process. ‘omics’ shift multiple the coordinated paradigm describing a and spatially require analyzing might fully a senescence Therefore, leaf be interactions. be understanding organ–organ to and to cell–cell expected includes needs Senescence perspective. also senescence dynamic is temporally Thus, a cellular from metabolism. of understood transitions and time-dependent physiology state, continuous single multiple a involves with not is controlled but senescence is Furthermore, senescence regulation. of leaf layers and that various it surprising genes and lifespan, not leaf information the multiple is throughout age signals of exogenous integrate and functions endogenous that collective pathways signaling the involves that of picture incomplete senescence. leaf an levels. underlying have multiple processes only molecular at currently acting we mechanisms Nevertheless, regulatory involves that codnl,i ilb ihyifraiet perform to informative highly be would modes. environments will regulatory different and it physiology in that senescence Accordingly, evolved expect different would have have we that therefore, plants and, strategy developmental that explored. aspect been important not another is has leaves senescent relocation from the nutrients controls of that mechanism The productivity, setting. plant or seed with components including integrated regulatory are the senescence how leaf know of yet networks not the entire do how the also understand within We to integrated plant. important systemically physiological an are death is and and It developmental senescence plant. is entire overall the cells the of dying by states affected in senescence Leaf also heterogeneity This leaf. entire is this states. the of how senescence heterogeneous the with of highly coordinated question in cells the are individual raises However, leaf age. senescing they within when death and senescence in. involved is transition ORE1 that age-dependent component-based modules the individual network in of here an exemplified from as their perspective, and than modules of rather network perspective of the interactions, networks, needed from RNA, molecular death are of and DNA, transitions efforts senescence leaf further between understand Therefore, to interactions metabolites. and here. complex proteins networks discussed encompass molecular as by executed that investigated are processes actively cellular However, be being should plant. are the inevitably process senescence in and strategy this life lifecycle the Hence, of plant stages. perspectives the the previous subsequent from of understood any and part to integral senescence linked an Thus, is lifecycle. death plants transitions However, age-associated their and states. developmental mostly throughout aged of has and series senesced senescence a undergo at leaf for only date, studied information To been processes. spatio-temporal understand better senescence obtain to the transitions to physiological and phenome morphological leaf the osdrn htla eecnei ihycmlxprocess complex highly a is senescence leaf that Considering utemr,la eecnei neouinrl acquired evolutionarily an is senescence leaf Furthermore, undergo collectively cells leaf that noted be also should It leaf regulate that components genetic and molecular The analyzing of importance the emphasize to like would We euaino efsnsec 4831 senescence leaf of Regulation Journal of Cell Science oe-odn . ems . rwr .B,Puech-Page B., P. Brewer, S., Fermas, V., Gomez-Roldan, esen . aei . ap .J,Hju,T,Nse,M . ai,I,Dor, I., Yariv, F., M. Nesher, T., Hajouj, J., M. Carp, G., Sabehi, S., Gepstein, M. Esteller, P. and F. Dunsmuir, M. Fraga, and J. Bedbrook, D., Bond-Nutter, M., J. F. Favreau, Slack, C., and Dean, S. S. Lee, M., Kato, K., Zhou, Z., Pincus, A., Lencastre, de C. C. Chusuei, and A. Volkov, T., Huynh, N., Ercal, W., Chen, avns,V,Lr,E,Kh,A n rg,M F. M. Fraga, and A. Kahn, E., Lara, V., Calvanese, uhnnWlatn . ae . arsn . ree . i,P . a,H G., H. Nam, O., P. Lim, E., Breeze, E., Harrison, T., Page, V., Buchanan-Wollaston, F. Slack, and M. Boehm, re,E . ars .J,Huwrh .G,Gen .M,Lea,D . Maro, S., D. Leeman, M., E. Green, G., A. Hauswirth, J., T. Maures, L., E. Greer, rsln .A,RsAvrzCnebr,A . ar .U,Rc,J . Hitchler, C., J. Rice, U., N. Nair, M., A. Alvarez-Canterbury, Rus A., J. Brusslan, S., Kiddle, C., Hill, R., Hickman, L., Hughes, S., McHattie, E., Harrison, E., Breeze, T. E. Palva, and J. Li, S., Besseau, B. Mueller-Roeber, and A. Wu, S., Balazadeh, ozl,S. Gonzalo, y . rlr . ice,A,Ulmn,R,Rue,G n ubc,K. Humbeck, and G. Reuter, R., Uhlemann, A., Fischer, K., Irmler, N., Ay, Le and J. Colombani, M., Bourouis, N., Arquier, References at http://jcs.biologists.org/lookup/suppl/doi:10.1242/jcs.109116/-/DC1 online available material Supplementary 2012R1A13004599]. 2010-0010915, Basic numbers National for [grant Research Science Institute the Program Basic of the and from Program CA1208]; number the Center [grant grants (IBS) of Research Science government by the the Korea: by supported of funded Republic was (NRF) Korea group of Foundation our Research in work The not Funding limitations. was space research to whose owing Commentary investigators this to in advance cited in apologize understand We to death. Acknowledgements required the networks. and senescence also at aging, organ are as including such level, and processes organisms, biological system cellular various and of molecular, molecular temporal and of studies the spatial evolution Comparative of of terms the in and transition program of death principles, will processes and physiological This regulatory senescence and strategy. metabolic their the senescence senescence, define distinct to a us allow with various plants of different studies comparative 4832 .P,Ltse . auoa . aon . oti,J .e al. et C. J. Portais, S., Danoun, R., Matusova, F., Letisse, P., J. genes. M. Bassani, and C. two of expression quantitative regulate genes. start rbcS translation petunia of downstream Sequences elegans. C. in longevity antagonize and 2159-2168. promote both MicroRNAs rnsGenet. 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Drosophila. in determination sex male-specific and span F. Elefant, ln J. Plant eaon .A,Si .adBue,A. Brunet, elegans. and Caenorhabditis in Y. longevity Shi, of inheritance A., B. Benayoun, 21) ui epnefco AF)pasamjrrl nrgltn auxin- regulating in role major a plays (ARF2) 2 longevity. leaf factor mediated response Auxin (2010). 229. Arabidopsis. in miR164 involving G. H. Nam, Arabidopsis. in 814-819. ARR2 of phosphorylation through I. Hwang, and G. H. stress ANAC019 Dev. of Ageing Mech. determinants and relationships signalling. structure-function K. family: Skriver, and C. in senescence and responses al. stress et in leaves. factors F. Arabidopsis transcription Bewicke-Copley, NAC three E., around Cooke, network A., Jackson, elegans. 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