Formation of the shoot apical meristem in Arabidopsis thaliana: an analysis of development in the wild type and in the shoot meristemless mutant

Development ◽  
1993 ◽  
Vol 119 (3) ◽  
pp. 823-831 ◽  
Author(s):  
M. K. Barton ◽  
R. S. Poethig

The primary shoot apical meristem of Arabidopsis is initiated late in embryogenesis, after the initiation of the cotyledons. We have identified a gene, called SHOOT MERISTEMLESS, which is critical for this process. shoot meristemless mutant seedlings lack a shoot apical meristem but are otherwise healthy and viable. The anatomy of mutant embryos demonstrates that the shoot meristemless-1 mutation completely blocks the initiation of the shoot apical meristem, but has no other obvious effects on embryo development. The failure of shoot meristemless tissue to regenerate shoots in tissue culture suggests that this gene regulates adventitious shoot meristem formation, as well as embryonic shoot meristem formation.

Development ◽  
1992 ◽  
Vol 116 (2) ◽  
pp. 397-403 ◽  
Author(s):  
H. M. Ottoline Leyser ◽  
I. J. Furner

The shoot apical meristem of dicotyledonous plants is highly regulated both structurally and functionally, but little is known about the mechanisms involved in this regulation. Here we describe the genetic and phenotypic characterisation of recessive mutations at three loci of Arabidopsis thaliana in which meristem structure and function are disrupted. The loci are Clavata1 (Clv1), Fasciata1 (Fas1) and Fasciata2 (Fas2). Plants mutant at these loci are fasciated having broad, flat stems and disrupted phyllotaxy. In all cases, the fasciations are associated with shoot apical meristem enlargement and altered floral development. While all the mutants share some phenotypic features they can be divided into two classes. The pleiotropic fas1 and fas2 mutants are unable to initiate wild- type organs, show major alterations in meristem structure and have reduced root growth. In contrast, clv1 mutant plants show near wild-type organ phenotypes, more subtle changes in shoot apical meristem structure and wild-type root growth.


Development ◽  
1993 ◽  
Vol 118 (3) ◽  
pp. 751-764 ◽  
Author(s):  
H. Tsukaya ◽  
S. Naito ◽  
G. P. Redei ◽  
Y. Komeda

We isolated and analyzed mutants of Arabidopsis thaliana, acaulis, with flower stalks that are almost absent or are much reduced in length. The mutations are divided between two loci, acaulis1 (acl1) and acaulis2 (acl2). The acl1-1 mutation has been assigned to linkage group 4 in the vicinity of locus ap2. The acl1-1 mutant showed premature arrest of the inflorescence meristem after the onset of reproductive development, followed by consequent reduction in the number of flower-bearing phytomers and therefore flowers. The apical meristem of the inflorescences was morphologically normal but its radius was about half that of the wild type. The acl1 mutants are also defective in the development of foliage leaves. Both defects could be rescued by growth at a specific temperature (28°C). The length of the cells in acl1-3 mutant was less than that in the wild type but the numbers of cells in leaves and internodes of acl1 mutants were calculated to be the same as those of the wild type. Thus, the defects in inflorescences and leaves were attributed to defects in the process of elongation (maturation) of these cells. Temperature-shift experiments showed that the Acl1+ product was necessary at all developmental stages. A critical stage was shown to exist for recovery from the cessation of development of inflorescence meristems that was caused by the acl1-1 mutation. Grafting experiments showed that the acl1-1 mutation does not affect diffusible substances. An analysis of double mutants carrying both acl1-1 and one of developmental mutations, ap1, clv1, lfy, or tfl1, showed that ACL1 is a new class of gene.


2015 ◽  
Vol 25 (1) ◽  
pp. 13-20
Author(s):  
Rindang Dwiyani ◽  
Aziz Purwantoro ◽  
Ari Indrianto ◽  
Endang Semiarti

KNOTED1?LIKE from Arabidopsis thaliana (KNAT1) gene keeps shoot apical meristem (SAM) in the meristematic state. The objective of the research was to investigate whether the function of KNAT1 gene in keeping plant cells under ‘meristematic state’ was functionally still work in the organ of the KNAT1 transformant. The transformant and WT plants were micropropagated, sliced and cut into some pieces, i.e. base of root, middle of root, root tip, a whole shoot, base of leaf, and leaf tip and planted in the New Phalaenopsis medium added with and without 5?M 2?iP and 0.15 ?M NAA. The results show that cells of KNAT1 transformant were more meristematic compared to wild type plants as the organ produced more buds in micropropagation.Plant Tissue Cult. & Biotech. 25(1): 13-20, 2015 (June)


Science ◽  
2013 ◽  
Vol 341 (6150) ◽  
pp. 1103-1106 ◽  
Author(s):  
Ruben Vanholme ◽  
Igor Cesarino ◽  
Katarzyna Rataj ◽  
Yuguo Xiao ◽  
Lisa Sundin ◽  
...  

Lignin is a major component of plant secondary cell walls. Here we describe caffeoyl shikimate esterase (CSE) as an enzyme central to the lignin biosynthetic pathway. Arabidopsis thaliana cse mutants deposit less lignin than do wild-type plants, and the remaining lignin is enriched in p-hydroxyphenyl units. Phenolic metabolite profiling identified accumulation of the lignin pathway intermediate caffeoyl shikimate in cse mutants as compared to caffeoyl shikimate levels in the wild type, suggesting caffeoyl shikimate as a substrate for CSE. Accordingly, recombinant CSE hydrolyzed caffeoyl shikimate into caffeate. Associated with the changes in lignin, the conversion of cellulose to glucose in cse mutants increased up to fourfold as compared to that in the wild type upon saccharification without pretreatment. Collectively, these data necessitate the revision of currently accepted models of the lignin biosynthetic pathway.


2020 ◽  
Author(s):  
Sharma Nidhi ◽  
Liu Tie

AbstractIn Arabidopsis, the genes SHOOT MERISTEMLESS (STM) and CLAVATA3 (CLV3) antagonistically regulate shoot meristem development. STM is essential for both development and maintenance of the meristem, as stm mutants fail to develop a shoot meristem during embryogenesis. CLV3, on the other hand, negatively regulates meristem proliferation, and clv3 mutants possess an enlarged shoot meristem. Genetic interaction studies revealed that stm and clv3 dominantly suppress each other’s phenotypes. STM works in conjunction with its closely related homologue KNOTTED1-LIKE HOMEOBOX GENE 6 (KNAT6) to promote meristem development and organ separation, as stm knat6 double mutants fail to form a meristem and produce a fused cotyledon. In this study, we show that clv3 fails to promote post-embryonic meristem formation in stm-1 background if we also remove KNAT6. stm-1 knat6 clv3 triple mutants result in early meristem termination and produce fused cotyledons similar to stm knat6 double mutant. Notably, the stm-1 knat6 and stm-1 knat6 clv3 alleles lack tissue in the presumed region of SAM. stm knat6 clv3 also showed reduced inflorescence size and shoot apex size as compared to clv3 single or stm clv3 double mutants. In contrast to previously published data, these data suggest that stm is epistatic to clv3 in postembryonic meristem development.HighlightSTM and KNAT6 genes determine post-embryonic meristem formation and activity in Arabidopsis. clv3 mutation is unable to rescue the stm knat6 meristemless phenotype.


Author(s):  
M.D. Sow ◽  
A-L. Le Gac ◽  
R. Fichot ◽  
S. Lanciano ◽  
A. Delaunay ◽  
...  

AbstractAs fixed and long living organisms subjected to repeated environmental stresses, trees have developed mechanisms such as phenotypic plasticity that help them to cope with fluctuating environmental conditions. Here, we tested the role DNA methylation as a hub of integration, linking plasticity and physiological response to water deficit in the shoot apical meristem of the model tree poplar (Populus). Using a reverse genetic approach, we compared hypomethylated RNAi-ddm1 lines to wild-type trees for drought tolerance. An integrative analysis was realized with phytohormone balance, methylomes, transcriptomes and mobilomes.Hypomethylated lines were more tolerant when subjected to moderate water deficit and were intrinsically more tolerant to drought-induced cavitation. The alteration of the DDM1 machinery induced variation in DNA methylation in a cytosine context dependent manner, both in genes and transposable elements. Hypomethylated lines subjected to water deficit showed altered expression of genes involved in phytohormone pathways, such as salicylic acid and modified hormonal balance. Several transposable elements showed stress- and/or line-specific patterns of reactivation, and we could detect copy number variations for two of them in stressed ddm1 lines.Overall, our data highlight two major roles for DNA methylation in the shoot apical meristem: control of stress response and plasticity through transduction of hormone signaling and maintenance of genome integrity through the control of transposable elements.


Development ◽  
2002 ◽  
Vol 129 (13) ◽  
pp. 3207-3217 ◽  
Author(s):  
Jean-Luc Gallois ◽  
Claire Woodward ◽  
G. Venugopala Reddy ◽  
Robert Sablowski

Almost all aerial parts of plants are continuously generated at the shoot apical meristem (SAM). To maintain a steady pool of undifferentiated cells in the SAM while continuously generating new organs, it is necessary to balance the rate of cell division with the rate of entrance into differentiation pathways. In the Arabidopsis meristem, SHOOT MERISTEMLESS (STM) and WUSCHEL (WUS) are necessary to keep cells undifferentiated and dividing. Here, we tested whether ectopic STM and WUS functions are sufficient to revert differentiation and activate cell division in differentiating tissues. Ectopic STM and WUS functions interacted non-additively and activated a subset of meristem functions, including cell division, CLAVATA1 expression and organogenesis, but not correct phyllotaxy or meristem self-maintenance. Our results suggest that WUS produces a non-cell autonomous signal that activates cell division in combination with STM and that combined WUS/STM functions can initiate the progression from stem cells to organ initiation.


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