Clonal analysis of the late flowering fca mutant of Arabidopsis thaliana: cell fate and cell autonomy

Development ◽  
1996 ◽  
Vol 122 (3) ◽  
pp. 1041-1050 ◽  
Author(s):  
I.J. Furner ◽  
J.F. Ainscough ◽  
J.A. Pumfrey ◽  
L.M. Petty
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Fate ◽  
Clonal Analysis ◽  
Wild Type ◽  
Fate Map ◽  
Plant Phenotype ◽  
X Irradiation ◽  
Cell Autonomy ◽  
Frequency Distance ◽  
Bolting And Flowering

Plants that are homozygous for the fca mutation bolt and flower later than wild-type (FCA) plants. The mutation has little or no effect on the fate map of the dry seed, except that the central cells give rise to further rosette leaves instead of the bolting stem, cauling leaves and inflorescence. The large and variable sectors affecting the late rosette leaves of fca plants were used to generate an abstract frequency-distance fate map of vegetative growth. The map relates the initiation of leaves in the plant apex to their final arrangements. The map was found to be a shallow dome with phyllotaxy superimposed on its surface. X-irradiation was used to provoke loss of the FCA allele from cells in heterozygous seeds. The resulting fca sectors had no effect on the plant phenotype. Even when L2 and L3 cells at the centre of the meristem could not produce the FCA gene product, bolting and flowering was unaffected. The genotypically fca mutant tissue was incorporated into phenotypically normal stems, cauline leaves and flowers. Possible reasons for the non-autonomous behaviour of the trait are discussed.

The effect of a heterochronic mutation, Teopod2, on the cell lineage of the maize shoot

Development ◽  
1991 ◽  
Vol 111 (3) ◽  
pp. 733-739 ◽  
Author(s):  
M. Dudley ◽  
R.S. Poethig
Keyword(s):  
Cell Division ◽  
Cell Fate ◽  
Structural Unit ◽  
Cell Lineage ◽  
Clonal Analysis ◽  
Wild Type ◽  
Dominant Mutation ◽  
Juvenile Phase ◽  
Basic Structural Unit ◽  
The Many

Teopod2 (Tp2) is a semi-dominant mutation of maize that prolongs the expression of characteristics normally confined to the juvenile phase of development. Two of the many dramatic morphological effects of this mutation are an increase in the number of vegetative nodes, and a reduction in the overall size of the shoot. To determine the cellular basis of these phenotypes, the technique of clonal analysis was used to compare the cell division patterns of wild-type and Tp2 plants. Our results indicate that Tp2 increases the number of vegetative nodes produced by the apicalmost cells in the meristem but does not affect the cell lineage of the basal, juvenile, part of the shoot. This result demonstrates that Tp2 does not act uniquely in a ‘juvenile’ domain of the meristem, but instead causes cells that are normally destined to produce adult structures to express juvenile traits inappropriately. Clonal analysis also demonstrates that Tp2 does not affect the size of the meristem prior to germination, nor does it affect the cell lineage of the basic structural unit of the stem, the phytomer. Thus the effects of this mutation on the size of the shoot are the result of changes in cell fate late in development.

Metabolic Regulation of Hippocampal Neuronal Development and Its Inhibition After Irradiation

2021 ◽  
Vol 80 (5) ◽  
pp. 467-475
Author(s):  
Yu-Qing Li ◽  
C Shun Wong
Keyword(s):  
Cell Fate ◽  
Metabolic Regulation ◽  
Energy Homeostasis ◽  
Neuronal Development ◽  
Adenosine Monophosphate ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Wild Type ◽  
Newborn Neuron ◽  
Negative Effect

Abstract 5′-Adenosine monophosphate-activated protein kinase (AMPK), a key regulator of cellular energy homeostasis, plays a role in cell fate determination. Whether AMPK regulates hippocampal neuronal development remains unclear. Hippocampal neurogenesis is abrogated after DNA damage. Here, we asked whether AMPK regulates adult hippocampal neurogenesis and its inhibition following irradiation. Adult Cre-lox mice deficient in AMPK in brain, and wild-type mice were used in a birth-dating study using bromodeoxyuridine to evaluate hippocampal neurogenesis. There was no evidence of AMPK or phospho-AMPK immunoreactivity in hippocampus. Increase in p-AMPK but not AMPK expression was observed in granule neurons and subgranular neuroprogenitor cells (NPCs) in the dentate gyrus within 24 hours and persisted up to 9 weeks after irradiation. AMPK deficiency in Cre-lox mice did not alter neuroblast and newborn neuron numbers but resulted in decreased newborn and proliferating NPCs. Inhibition of neurogenesis was observed after irradiation regardless of genotypes. In Cre-lox mice, there was further loss of newborn early NPCs and neuroblasts but not newborn neurons after irradiation compared with wild-type mice. These results are consistent with differential negative effect of AMPK on hippocampal neuronal development and its inhibition after irradiation.

scholarly journals cot1: A Regulator of Arabidopsis Trichome Initiation

Genetics ◽  
1998 ◽  
Vol 149 (2) ◽  
pp. 565-577
Author(s):  
Daniel B Szymanski ◽  
Daniel A Klis ◽  
John C Larkin ◽  
M David Marks
Keyword(s):  
Cell Fate ◽  
Gene Dosage ◽  
Signal Transduction Pathway ◽  
Spatial Arrangement ◽  
Complex Signal ◽  
Chromosome 2 ◽  
Wild Type ◽  
Trichome Formation ◽  
In The Wild ◽  
Leaf Trichome

Abstract In Arabidopsis, the timing and spatial arrangement of trichome initiation is tightly regulated and requires the activity of the GLABROUS1 (GL1) gene. The COTYLEDON TRICHOME 1 (COT1) gene affects trichome initiation during late stages of leaf development and is described in this article. In the wild-type background, cot1 has no observable effect on trichome initiation. GL1 overexpression in wild-type plants leads to a modest number of ectopic trichomes and to a decrease in trichome number on the adaxial leaf surface. The cot1 mutation enhances GL1-overexpression-dependent ectopic trichome formation and also induces increased leaf trichome initiation. The expressivity of the cot1 phenotype is sensitive to cot1 and 35S::GL1 gene dosage, and the most severe phenotypes are observed when cot1 and 35S::GL1 are homozygous. The COT1 locus is located on chromosome 2 15.3 cM north of er. Analysis of the interaction between cot1, try, and 35S::GL1 suggests that COT1 is part of a complex signal transduction pathway that regulates GL1-dependent adoption of the trichome cell fate.

scholarly journals Inhibition of cell expansion enhances cortical microtubule stability in the root apex of Arabidopsis thaliana

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Veronica Giourieva ◽  
Emmanuel Panteris
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Wall ◽  
Cell Expansion ◽  
Cortical Microtubule ◽  
Root Apex ◽  
Cellulose Synthase ◽  
Cellulose Biosynthesis ◽  
Cortical Microtubules ◽  
Wild Type ◽  
Microtubule Stability

Abstract Background Cortical microtubules regulate cell expansion by determining cellulose microfibril orientation in the root apex of Arabidopsis thaliana. While the regulation of cell wall properties by cortical microtubules is well studied, the data on the influence of cell wall to cortical microtubule organization and stability remain scarce. Studies on cellulose biosynthesis mutants revealed that cortical microtubules depend on Cellulose Synthase A (CESA) function and/or cell expansion. Furthermore, it has been reported that cortical microtubules in cellulose-deficient mutants are hypersensitive to oryzalin. In this work, the persistence of cortical microtubules against anti-microtubule treatment was thoroughly studied in the roots of several cesa mutants, namely thanatos, mre1, any1, prc1-1 and rsw1, and the Cellulose Synthase Interacting 1 protein (csi1) mutant pom2-4. In addition, various treatments with drugs affecting cell expansion were performed on wild-type roots. Whole mount tubulin immunolabeling was applied in the above roots and observations were performed by confocal microscopy. Results Cortical microtubules in all mutants showed statistically significant increased persistence against anti-microtubule drugs, compared to those of the wild-type. Furthermore, to examine if the enhanced stability of cortical microtubules was due to reduced cellulose biosynthesis or to suppression of cell expansion, treatments of wild-type roots with 2,6-dichlorobenzonitrile (DCB) and Congo red were performed. After these treatments, cortical microtubules appeared more resistant to oryzalin, than in the control. Conclusions According to these findings, it may be concluded that inhibition of cell expansion, irrespective of the cause, results in increased microtubule stability in A. thaliana root. In addition, cell expansion does not only rely on cortical microtubule orientation but also plays a regulatory role in microtubule dynamics, as well. Various hypotheses may explain the increased cortical microtubule stability under decreased cell expansion such as the role of cell wall sensors and the presence of less dynamic cortical microtubules.

scholarly journals Increased Notch 1 Expression and Attenuated Stimulatory G Protein Coupling to Adenylyl Cyclase in Osteonectin-Null Osteoblasts

Endocrinology ◽  
2007 ◽  
Vol 148 (4) ◽  
pp. 1666-1674 ◽  
Author(s):  
Catherine B. Kessler ◽  
Anne M. Delany
Keyword(s):  
Adenylyl Cyclase ◽  
G Protein ◽  
Cell Fate ◽  
Osteoblastic Cells ◽  
Matricellular Protein ◽  
Wild Type ◽  
Notch 1 ◽  
Matrix Assembly ◽  
G Protein Coupling ◽  
Protein Coupling

Osteonectin, or secreted protein acidic and rich in cysteine, is one of the most abundant noncollagen matrix components in bone. This matricellular protein regulates extracellular matrix assembly and maturation in addition to modulating cell behavior. Mice lacking osteonectin develop severe low-turnover osteopenia, and in vitro studies of osteonectin-null osteoblastic cells showed that osteonectin supports osteoblast formation, maturation, and survival. The present studies demonstrate that osteonectin-null osteoblastic cells have increased expression of Notch 1, a well-documented regulator of cell fate in multiple systems. Furthermore, osteonectin-null cells are more plastic and less committed to osteoblastic differentiation, able to pursue adipogenic differentiation given the appropriate signals. Notch 1 transcripts are down-regulated by inducers of cAMP in both wild-type and osteonectin-null osteoblasts, suggesting that the mutant osteoblasts may have a defect in generation of cAMP in response to stimuli. Indeed, many bone anabolic agents signal through increased cAMP. Wild-type and osteonectin-null osteoblasts generated comparable amounts of cAMP in response to forskolin, a direct stimulator of adenylyl cyclase. However, the ability of osteonectin-null osteoblasts to generate cAMP in response to cholera toxin, a direct stimulator of Gs, was attenuated. These data imply that osteonectin-null osteoblasts have decreased coupling of Gs to adenylyl cyclase. Because osteonectin promotes G protein coupling to an effector, our studies support the concept that low-turnover osteopenia can result from reducing G protein coupled receptor activity.

Caffeoyl Shikimate Esterase (CSE) Is an Enzyme in the Lignin Biosynthetic Pathway in Arabidopsis

Science ◽  
2013 ◽  
Vol 341 (6150) ◽  
pp. 1103-1106 ◽  
Author(s):  
Ruben Vanholme ◽  
Igor Cesarino ◽  
Katarzyna Rataj ◽  
Yuguo Xiao ◽  
Lisa Sundin ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Walls ◽  
Metabolite Profiling ◽  
Biosynthetic Pathway ◽  
Wild Type ◽  
Secondary Cell Walls ◽  
Phenolic Metabolite ◽  
In The Wild ◽  
Lignin Biosynthetic Pathway

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.

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