The WUSCHEL gene is required for shoot and floral meristem integrity in Arabidopsis

Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 87-96 ◽  
Author(s):  
T. Laux ◽  
K.F. Mayer ◽  
J. Berger ◽  
G. Jurgens
Keyword(s):  
Developmental Stages ◽  
Shoot Meristem ◽  
Wild Type ◽  
Recessive Mutations ◽  
Organ Identity ◽  
Flat Structures ◽  
Meristem Identity ◽  
Wus Gene ◽  
Floral Meristems ◽  
Shoot Meristems

Self perpetuation of the shoot meristem is essential for the repetitive initiation of shoot structures during plant development. In Arabidopsis shoot meristem maintenance is disrupted by recessive mutations in the WUSCHEL (WUS) gene. The defect is evident at all developmental stages and is restricted to shoot and floral meristems, whereas the root meristem is not affected. wus mutants fail to properly organize a shoot meristem in the embryo. Postembryonically, defective shoot meristems are initiated repetitively but terminate prematurely in aberrant flat structures. In contrast to wild-type shoot meristems, primordia initiation occurs ectopically across mutant apices, including the center, and often new shoot meristems instead of organs are initiated. The cells of wus shoot apices are larger and more vacuolated than wild-type shoot meristem cells. wus floral meristems terminate prematurely in a central stamen. Double mutant studies indicate that the number of organ primordia in the center of wus flowers is limited, irrespective of organ identity and we propose that meristem cells are allocated into floral whorl domains in a sequential manner. WUS activity also appears to be required for the formation of supernumerary organs in the center of agamous, superman or clavata1 flowers, suggesting that the WUS gene acts upstream of the corresponding genes. Our results suggest that the WUS gene is specifically required for central meristem identity of shoot and floral meristems to maintain their structural and functional integrity.

scholarly journals Mutations in the PERIANTHIA gene of Arabidopsis specifically alter floral organ number and initiation pattern

Development ◽  
1996 ◽  
Vol 122 (4) ◽  
pp. 1261-1269 ◽  
Author(s):  
M.P. Running ◽  
E.M. Meyerowitz
Keyword(s):  
Floral Organ ◽  
Floral Meristem ◽  
Wild Type ◽  
Organ Identity ◽  
The Family ◽  
Dividing Cells ◽  
Meristem Identity ◽  
Plant Families ◽  
Open Question ◽  
Floral Organ Identity Genes

An open question in developmental biology is how groups of dividing cells can generate specific numbers of segments or organs. We describe the phenotypic effects of mutations in PERIANTHIA, a gene specifically required for floral organ patterning in Arabidopsis thaliana. Most wild-type Arabidopsis flowers have 4 sepals, 4 petals, 6 stamens, and 2 carpels. Flowers of perianthia mutant plants most commonly show a pentamerous pattern of 5 sepals, 5 petals 5 stamens, and 2 carpels. This pattern is characteristic of flowers in a number of plant families, but not in the family Brassicaceae, which includes Arabidopsis. Unlike previously described mutations affecting floral organ number, perianthia does not appear to affect apical or floral meristem sizes, nor is any other aspect of vegetative or floral development severely affected. Floral organs in perianthia arise in a regular, stereotypical pattern similar to that in distantly related species with pentamerous flowers. Genetic analysis shows that PERIANTHIA acts downstream of the floral meristem identity genes and independently of the floral meristem size and floral organ identity genes in establishing floral organ initiation patterns. Thus PERIANTHIA acts in a previously unidentified process required for organ patterning in Arabidopsis flowers.

scholarly journals MAX1 and MAX2 control shoot lateral branching in Arabidopsis

Development ◽  
2002 ◽  
Vol 129 (5) ◽  
pp. 1131-1141 ◽  
Author(s):  
Petra Stirnberg ◽  
Karin van de Sande ◽  
H. M. Ottoline Leyser
Keyword(s):  
Positional Cloning ◽  
Leaf Shape ◽  
Shoot Meristem ◽  
Axillary Shoot ◽  
Axillary Meristem ◽  
Axillary Shoots ◽  
Recessive Mutations ◽  
Lateral Shoots ◽  
Plant Shoots ◽  
Shoot Meristems

Plant shoots elaborate their adult form by selective control over the growth of both their primary shoot apical meristem and their axillary shoot meristems. We describe recessive mutations at two loci in Arabidopsis, MAX1 and MAX2, that affect the selective repression of axillary shoots. All the first order (but not higher order) axillary shoots initiated by mutant plants remain active, resulting in bushier shoots than those of wild type. In vegetative plants where axillary shoots develop in a basal to apical sequence, the mutations do not clearly alter node distance, from the shoot apex, at which axillary shoot meristems initiate but shorten the distance at which the first axillary leaf primordium is produced by the axillary shoot meristem. A small number of mutant axillary shoot meristems is enlarged and, later in development, a low proportion of mutant lateral shoots is fasciated. Together, this suggests that MAX1 and MAX2 do not control the timing of axillary meristem initiation but repress primordia formation by the axillary meristem. In addition to shoot branching, mutations at both loci affect leaf shape. The mutations at MAX2 cause increased hypocotyl and petiole elongation in light-grown seedlings. Positional cloning identifies MAX2 as a member of the F-box leucine-rich repeat family of proteins. MAX2 is identical to ORE9, a proposed regulator of leaf senescence (Woo, H. R., Chung, K. M., Park, J.-H., Oh, S. A., Ahn, T., Hong, S. H., Jang, S. K. and Nam, H. G. (2001) Plant Cell13, 1779-1790). Our results suggest that selective repression of axillary shoots involves ubiquitin-mediated degradation of as yet unidentified proteins that activate axillary growth.

Expression of floricaula in single cell layers of periclinal chimeras activates downstream homeotic genes in all layers of floral meristems

Development ◽  
1995 ◽  
Vol 121 (1) ◽  
pp. 27-35 ◽  
Author(s):  
S.S. Hantke ◽  
R. Carpenter ◽  
E.S. Coen
Keyword(s):  
Cell Layer ◽  
Homeotic Genes ◽  
Expression Domain ◽  
Phenotypic Properties ◽  
Organ Identity ◽  
Cell Layers ◽  
Periclinal Chimeras ◽  
Meristem Identity ◽  
Cell Autonomy ◽  
Floral Meristems

We show that the flowering sectors on plants mutant for floricaula (flo), a meristem identity gene in Antirrhinum majus, are periclinal chimeras expressing flo in either the L1, L2 or L3 cell layer. Flower morphology is almost normal in L1 chimeras, but altered in L2 and L3 chimeras. Expression of flo in any one cell layer results in the expression of organ identity genes, deficiens (def) and plena (ple) in all three cell layers of the chimeras, showing that flo acts inductively to promote gene transcription. The activation of both def and ple is delayed, and the expression domain of def is reduced, accounting for some of the phenotypic properties of the chimeras. Furthermore, we show that flo exhibits some cell-autonomy with respect to autoregulation.

scholarly journals CLAVATA1, a regulator of meristem and flower development in Arabidopsis

Development ◽  
1993 ◽  
Vol 119 (2) ◽  
pp. 397-418 ◽  
Author(s):  
S.E. Clark ◽  
M.P. Running ◽  
E.M. Meyerowitz
Keyword(s):  
Flower Development ◽  
Double Mutant ◽  
Apical Meristem ◽  
Expression Patterns ◽  
Floral Meristem ◽  
Homeotic Genes ◽  
Wild Type ◽  
Meristem Identity ◽  
Floral Meristems ◽  
Transition To Flowering

We have investigated the effects on plant development of mutations in the Arabidopsis thaliana CLAVATA1 gene. In clavata1 plants, vegetative, inflorescence and floral meristems are all enlarged relative to wild type. The apical meristem can fasciate in the more severe mutant alleles, and this fasciation can occur prior to the transition to flowering. Flowers of clavata1 plants can have increased numbers of organs in all four whorls, and can also have additional whorls not present in wild-type flowers. Double mutant combinations of clavata1 with agamous, apetala2, apetala3 and pistillata indicate that CLAVATA1 controls the underlying floral meristem structure upon which these homeotic genes act. Double mutant combinations of clavata1 with apetala1 and leafy indicate CLAVATA1 plays a role in establishing and maintaining floral meristem identity, in addition to its role in controlling meristem size. In support of this, RNA expression patterns of AGAMOUS and APETALA1 are altered in clavata1 flowers.

scholarly journals Mutants of downy mildew resistance in Lactuca sativa (lettuce).

Genetics ◽  
1994 ◽  
Vol 137 (3) ◽  
pp. 867-874
Author(s):  
P A Okubara ◽  
P A Anderson ◽  
O E Ochoa ◽  
R W Michelmore
Keyword(s):  
Molecular Marker ◽  
Downy Mildew ◽  
Genomic Dna ◽  
Spontaneous Mutation ◽  
Multigene Families ◽  
Downy Mildew Resistance ◽  
Bremia Lactucae ◽  
Wild Type ◽  
Mildew Resistance ◽  
Recessive Mutations

Abstract As part of our investigation of disease resistance in lettuce, we generated mutants that have lost resistance to Bremia lactucae, the casual fungus of downy mildew. Using a rapid and reliable screen, we identified 16 distinct mutants of Latuca sativa that have lost activity of one of four different downy mildew resistance genes (Dm). In all mutants, only a single Dm specificity was affected. Genetic analysis indicated that the lesions segregated as single, recessive mutations at the Dm loci. Dm3 was inactivated in nine of the mutants. One of five Dm 1 mutants was selected from a population of untreated seeds and therefore carried a spontaneous mutation. All other Dm1, Dm3, Dm5/8 and Dm7 mutants were derived from gamma- or fast neutron-irradiated seed. In two separate Dm 1 mutants and in each of the eight Dm3 mutants analyzed, at least one closely linked molecular marker was absent. Also, high molecular weight genomic DNA fragments that hybridized to a tightly linked molecular marker in wild type were either missing entirely or were truncated in two of the Dm3 mutants, providing additional evidence that deletions had occurred in these mutants. Absence of mutations at loci epistatic to the Dm genes suggested that such loci were either members of multigene families, were critical for plant survival, or encoded components of duplicated pathways for resistance; alternatively, the genes determining downy mildew resistance might be limited to the Dm loci.

scholarly journals GENE INTERACTIONS BETWEEN POTASSIUM-SENSITIVE AND POTASSIUM-RESISTANT MUTATIONS OF PARAMECIUM TETRAURELIA

Genetics ◽  
1983 ◽  
Vol 103 (2) ◽  
pp. 153-160
Author(s):  
Donald L Cronkite
Keyword(s):  
High Resistance ◽  
Gene Interactions ◽  
Paramecium Tetraurelia ◽  
Wild Type ◽  
Recessive Mutations ◽  
Resistant Genes ◽  
Type Gene ◽  
Moderately Resistant

ABSTRACT Two unlinked recessive mutations (ks-1 and ks-2) have been induced in Paramecium tetraurelia stock 51. Wild-type survives and grows when up to 30 mm KCl is added to the medium, but the mutants cease to grow and die when added KCl reaches 20-25 m m. These K+-sensitives have been crossed to stocks containing the K+-resistant genes, fA (very resistant) and kA(moderately resistant). All four genes are unlinked. Double mutants of ks-1 and either kA or fA are as resistant as the resistant member of the pair. Doubles of ks-2 and kA are like wild type, and doubles of ks-2 and fA are shifted from high resistance toward wild type. Gene ks-2 acts like a suppressor of kA and fA. This suppression can be understood in terms of the known biochemical defects of the mutants.

16. Physiological effects of IDH1 loss-of-function on Chondrocyte Differentiation through Hedgehog Pathway upregulation

2018 ◽  
Author(s):  
Cassie Tyson
Keyword(s):  
Developmental Stages ◽  
Hedgehog Pathway ◽  
Chondrocyte Differentiation ◽  
Loss Of Function ◽  
Wild Type ◽  
Phenotypic Analysis ◽  
Growth Plate Chondrocytes ◽  
Idh Mutations ◽  
Cartilage Tumors ◽  
Deficient Mice

Cartilage tumors are the most common and terminal primary neoplasms in bone. Physiologically, bones formed through endochondral ossification are regulated by the Hedgehog pathway and Parathyroid hormone-like hormone feedback loop. The upregulation of the infamous Hedgehog pathway has been demonstrated in several non-cartilaginous neoplasms. Recently, frequent mutational events of isocitrate dehydrogenase1 (IDH1) were identified in cartilage tumors. In other neoplasms, IDH mutations produces an oncometabolite that can promote HIF1a activation, contributing to tumorigenesis. Currently, the role of IDH1 mutations in cartilage tumors remain unknown. Investigating the physiological aspect of IDH1proves useful in identifying novel therapeutic targets for cartilage tumors. IDH1 deficient and wild-type littermates, were harvested for forelimbs and hindlimbs at various developmental stages for phenotypic analysis via hematoxylin and eosin staining. Histological analysis demonstrated IDH1 homozygous deficient mice at embryonic stages exhibited dwarfism and an elongated layer of hypertrophic chondrocytes. This was verified via immunohistochemistry Type 10 Collagen staining and Quantitative PCR (qPCR) using the chondrocyte terminal differentiation marker Col10a1. Whole skeletons of IDH1 deficient mice were subjected to skeletal double staining which demonstrated delayed mineralization of underdeveloped IDH1 deficient mice contrasted with wild-type littermates. qPCR was performed to examine the status of chondrocyte differentiation through the Hedgehog pathway in cultured primarymouse growth plate chondrocytes. Interestingly, IDH1 deficient non-neoplastic cells revealed significant upregulation of Hedgehog target molecules in IDH1 deficient chondrocytes. As a result, the loss-offunction of IDH1 was identified as a potential impairment of chondrocyte differentiation and a factor towards chondrocyte tumorgenisis.

scholarly journals Phospholipid flippases enable precursor B cells to flee engulfment by macrophages

2018 ◽  
Vol 115 (48) ◽  
pp. 12212-12217 ◽  
Author(s):  
Katsumori Segawa ◽  
Yuichi Yanagihashi ◽  
Kyoko Yamada ◽  
Chigure Suzuki ◽  
Yasuo Uchiyama ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
B Cells ◽  
B Cell ◽  
Developmental Stages ◽  
Peritoneal Macrophages ◽  
Dependent Manner ◽  
Wild Type ◽  
Immature B Cells ◽  
T Lymphoma ◽  
Precursor B Cells

ATP11A and ATP11C, members of the P4-ATPases, are flippases that translocate phosphatidylserine (PtdSer) from the outer to inner leaflet of the plasma membrane. Using the W3 T lymphoma cell line, we found that Ca2+ ionophore-induced phospholipid scrambling caused prolonged PtdSer exposure in cells lacking both the ATP11A and ATP11C genes. ATP11C-null (ATP11C−/y) mutant mice exhibit severe B-cell deficiency. In wild-type mice, ATP11C was expressed at all B-cell developmental stages, while ATP11A was not expressed after pro−B-cell stages, indicating that ATP11C−/y early B-cell progenitors lacked plasma membrane flippases. The receptor kinases MerTK and Axl are known to be essential for the PtdSer-mediated engulfment of apoptotic cells by macrophages. MerTK−/− and Axl−/− double deficiency fully rescued the lymphopenia in the ATP11C−/y bone marrow. Many of the rescued ATP11C−/y pre-B and immature B cells exposed PtdSer, and these cells were engulfed alive by wild-type peritoneal macrophages, in a PtdSer-dependent manner. These results indicate that ATP11A and ATP11C in precursor B cells are essential for rapidly internalizing PtdSer from the cell surface to prevent the cells’ engulfment by macrophages.

INHERITANCE OF RADIATION-INDUCED SPINAL CURVATURES IN THE GUPPY LEBISTES RETICULATUS

1969 ◽  
Vol 11 (4) ◽  
pp. 937-947 ◽  
Author(s):  
Johannes Horst Schröder
Keyword(s):  
Germ Cells ◽  
Vertebral Column ◽  
Segregation Ratio ◽  
X Rays ◽  
Wild Type ◽  
Spinal Curvatures ◽  
Recessive Mutations ◽  
Quantitative Characters ◽  
Radiation Induced ◽  
Lebistes Reticulatus

Hereditary changes in the shape of the vertebral column in Lebistes reticulatus appeared after ancestral irradiation of immature germ cells with 500 or 1000 R of X-rays. Although the mutant to wild-type ratios in the F2 generation after outcrossing fitted a digenic and a trigenic segregation ratio, respectively, the quantitative characters in question are assumed to be caused by recessive mutations of polygenes which are highly mutable.

Ultrastructural analysis of Drosophila ovarian follicles differing in yolk polypeptide (yps) composition

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 319-328
Author(s):  
F. Giorgi ◽  
P. Lucchesi ◽  
A. Morelli ◽  
M. Bownes
Keyword(s):  
Golgi Apparatus ◽  
Juvenile Hormone ◽  
Developmental Stages ◽  
Ovarian Follicles ◽  
Endocytic Pathway ◽  
Intermediate Cell ◽  
Wild Type ◽  
Vesicular Traffic

Drosophila ovarian follicles were examined ultrastructurally to study the vesicular traffic in the cortical ooplasm. The endocytic pathway leading to the production of yolk spheres was visualized following in vivo or in vitro exposure to peroxidase. The Golgi apparatus and the yolk spheres of wild-type ovarian follicles were preferentially labelled by fixation with osmium zinc iodide (OZI). Labelling of wild-type ovarian follicles was compared to that of several mutant follicles--L186/Basc, fs(2)A17 and ap4--which are defective in vitellogenesis. In these mutants, the Golgi apparatus and the vesicles nearby were either scantly labelled or not labelled at all. In oocytes from flies homozygous for the gene fs(1)1163, the Golgi apparatus was labelled as in the controls, but no yolk spheres appeared to be labelled with OZI at any of the developmental stages. In several Drosophila strains, the pattern of OZI label in the cortical ooplasm was seen to vary in relation to the number of yp structural genes. In starved Drosophila females, OZI labelling of the cortical ooplasm appeared restricted to the Golgi apparatus and to an extended tubular network. A similar labelling pattern was also detected in in vitro cultured vitellogenic follicles. Refeeding, topical application of juvenile hormone analogue to starved females or hormone addition to the culture medium, all caused the yolk spheres to become labelled with OZI and to incorporate peroxidase. These observations prove that impairing endocytic uptake by either mutation or lack of juvenile hormone prevents fusion of coated vesicles and tubules with the yolk spheres and leads them instead to form an intermediate cell compartment with Golgi-derived vesicles.

Sign in / Sign up

Export Citation Format

Share Document