scholarly journals Loss-of-function mutations in the maize homeobox gene, knotted1, are defective in shoot meristem maintenance

Development ◽  
1997 ◽  
Vol 124 (16) ◽  
pp. 3045-3054 ◽  
Author(s):  
R.A. Kerstetter ◽  
D. Laudencia-Chingcuanco ◽  
L.G. Smith ◽  
S. Hake
Keyword(s):  
Homeobox Gene ◽  
Leaf Primordia ◽  
Shoot Meristem ◽  
Loss Of Function ◽  
Floral Organs ◽  
Leaf Phenotype ◽  
Lateral Organ ◽  
Recessive Mutant ◽  
Meristem Maintenance ◽  
Shoot Meristems

The product of the maize homeobox gene, knotted1 (kn1), localizes to the nuclei of cells in shoot meristems, but is absent from portions of the meristem where leaf primordia or floral organs initiate. Recessive mutant alleles of kn1 were obtained by screening for loss of the dominant leaf phenotype in maize. Mutant kn1 alleles carrying nonsense, splicing and frame shift mutations cause severe inflorescence and floral defects. Mutant tassels produce fewer branches and spikelets. Ears are often absent, and when present, are small with few spikelets. In addition, extra carpels form in female florets and ovule tissue proliferates abnormally. Less frequently, extra leaves form in the axils of vegetative leaves. These mutations reveal a role for kn1 in meristem maintenance, particularly as it affects branching and lateral organ formation.

Control of phyllotaxy in maize by the abphyl1 gene

Development ◽  
1999 ◽  
Vol 126 (2) ◽  
pp. 315-323 ◽  
Author(s):  
D. Jackson ◽  
S. Hake
Keyword(s):  
Apical Meristem ◽  
General Structure ◽  
Homeobox Gene ◽  
The Other ◽  
Shoot Meristem ◽  
Regular Pattern ◽  
Expression Domain ◽  
Geometric Patterns ◽  
Maize Plants ◽  
Shoot Meristems

Organogenesis in plants occurs at the shoot apical meristem, a group of indeterminate stem cells that are organized during embryogenesis. Regulated initiation of leaves or flowers from the shoot meristem gives rise to the familiar geometric patterns observed throughout the plant kingdom. The mechanism by which these patterns, termed phyllotaxies, are generated, remains unclear. Maize plants initiate leaves singly, alternating from one side to the other in a regular pattern. Here we describe a recessive maize mutant, abphyl1, that initiates leaves in opposite pairs, in a pattern termed decussate phyllotaxy. The decussate shoot meristems are larger than normal throughout development, though the general structure and organization of the meristem is not altered. abph1 mutants are first distinguished during embryogenesis, prior to true leaf initiation, by a larger shoot meristem and coincident larger expression domain of the homeobox gene knotted1. Therefore, the abph1 gene regulates morphogenesis in the embryo, and plays a role in determining the phyllotaxy of the shoot.

Shoot meristem size is dependent on inbred background and presence of the maize homeobox gene, knotted1

Development ◽  
2000 ◽  
Vol 127 (14) ◽  
pp. 3161-3172 ◽  
Author(s):  
E. Vollbrecht ◽  
L. Reiser ◽  
S. Hake
Keyword(s):  
Gene Function ◽  
Apical Meristem ◽  
Homeobox Gene ◽  
Shoot Meristem ◽  
Dominant Allele ◽  
Element Analysis ◽  
Meristem Size ◽  
Recessive Mutations ◽  
Undifferentiated State ◽  
Meristem Maintenance

The knotted1 (kn1) gene of maize is expressed in meristems and is absent from leaves, including the site of leaf initiation within the meristem. Recessive mutations of kn1 have been described that limit the capacity to make branches and result in extra carpels. Dominant mutations suggest that kn1 function plays a role in maintaining cells in an undifferentiated state. We took advantage of a Ds-induced dominant allele in order to screen for additional recessive alleles resulting from mobilization of the Ds element. Analysis of one such allele revealed a novel embryonic shoot phenotype in which the shoot initiated zero to few organs after the cotyledon was made, resulting in plants that arrested as seedlings. We refer to this phenotype as a limited shoot. The limited shoot phenotype reflected loss of kn1 function, but its penetrance was background dependent. We examined meristem size and found that plants lacking kn1 function had shorter meristems than non-mutant siblings. Furthermore, meristems of restrictive inbreds were significantly shorter than meristems of permissive inbreds, implying a correlation between meristem height and kn1 gene function in the embryo. Analysis of limited shoot plants during embryogenesis indicated a role for kn1 in shoot meristem maintenance. We discuss a model for kn1 in maintenance of the morphogenetic zone of the shoot apical meristem.

ESCAPE FROM MATING-TYPE INCOMPATIBILITY IN BISEXUAL (A + a) NEUROSPORA HETEROKARYONS

1975 ◽  
Vol 17 (3) ◽  
pp. 441-449 ◽  
Author(s):  
A. M. DeLange ◽  
A. J. F. Griffiths
Keyword(s):  
Mating Type ◽  
Loss Of Function ◽  
Wild Type ◽  
Opposite Mating Type ◽  
Type Locus ◽  
Heterokaryon Incompatibility ◽  
Recessive Mutant ◽  
Type Rate ◽  
Wild Type Rate ◽  
Incompatibility Locus

In Neurospora crassa, strains of opposite mating type generally do not form stable heterokaryons because the mating type locus acts as a heterokaryon incompatibility locus. However, when one A and one a strain, having complementing auxotrophic mutants, are placed together on minimal medium, growth may occur, although the growth is generally slow. In this study, escape from such slow growth to that at a wild type or near-wild type rate was observed. The escaped cultures are stable heterokaryons, mostly having lost the mating type allele function from one component nucleus, so that the nuclear types are heterokaryon compatible. Either A or a mating type can be lost. This loss of function has been attributed to deletion since only one nuclear type could be recovered in all heterokaryons except one, but deletion spanning adjacent loci has been directly demonstrated in a minority of cases. Alternatively when one component strain is tol and the other tol+ (tol being a recessive mutant suppressing the heterokaryon incompatibility associated with mating type), escape may occur by the deletion or mutation of tol+, also resulting in heterokaryon compatibility. An induction mechanism for escape is speculated upon.

scholarly journals Extended expression of MaKN1 contributes to the leaf morphology in aquatic forms of Myriophyllum aquaticum

Botany ◽  
2015 ◽  
Vol 93 (9) ◽  
pp. 611-621
Author(s):  
M.D. Shafiullah ◽  
Christian R. Lacroix
Keyword(s):  
Apical Meristem ◽  
Leaf Morphology ◽  
Expression Patterns ◽  
Homeobox Gene ◽  
Leaf Primordia ◽  
Leaf Primordium ◽  
Myriophyllum Aquaticum ◽  
Knox Gene ◽  
Leaf Morphogenesis

Myriophyllum aquaticum (Vell.) Verdc. is heterophyllous in nature with highly dissected simple leaves consisting of several lobes. KNOX (KNOTTED1-LIKE HOMEOBOX) genes are believed to have played an important role in the evolution of leaf diversity. Up-regulation of KNOX during leaf primordium initiation can lead to leaf dissection in plants with simple leaves and, if overexpressed, can produce ectopic meristems on leaves. A previous study on KNOX gene expression in the aerial form of this species showed that this gene is expressed in the shoot apical meristem (SAM), as well as in leaf primordia P0 to P8. Based on these results, it was hypothesized that the prolonged expression of the MaKN1 (Myriophyllum aquaticum Knotted1-like homeobox) gene beyond P8, might play an important role in the generation of more lobes, longer lobes, and hydathode formation in the aquatic leaves of M. aquaticum. The technique of in situ hybridization was carried out using a previously sequenced 300 bp fragment of MaKN1 to determine the expression patterns of this gene in the shoot of aquatic forms of the plant. Expression patterns of MaKN1 revealed that the SAM and leaf primordia of aquatic forms of M. aquaticum at levels P0 (youngest) to P4 were distributed throughout these structures. The level of expression of this MaKN1 gene progressively became more localized to lobes in older leaf primordia (levels P5 to P12). Previous studies of aerial forms of this plant showed MaKN1 expression until P8. Our results with aquatic forms show that the highly dissected leaf morphology in aquatic forms was the result of the prolonged expression of MaKN1 beyond P8. This resulted in the formation of elongated and slightly more numerous lobes, and hydathodes in aquatic forms. These findings support the view that KNOX genes are important developmental regulators of leaf morphogenesis and have played an important role in the evolution of leaf forms in the plant kingdom.

scholarly journals Author response: Mechanical stress contributes to the expression of the STM homeobox gene in Arabidopsis shoot meristems

2015 ◽  
Author(s):  
Benoît Landrein ◽  
Annamaria Kiss ◽  
Massimiliano Sassi ◽  
Aurélie Chauvet ◽  
Pradeep Das ◽  
...  
Keyword(s):  
Mechanical Stress ◽  
Homeobox Gene ◽  
Author Response ◽  
Shoot Meristems

scholarly journals A nervous system-specific subnuclear organelle in Caenorhabditis elegans

Genetics ◽  
2021 ◽  
Vol 217 (1) ◽  
Author(s):  
Kenneth Pham ◽  
Neda Masoudi ◽  
Eduardo Leyva-Díaz ◽  
Oliver Hobert
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Homeobox Gene ◽  
Cell Types ◽  
Nuclear Bodies ◽  
Loss Of Function ◽  
Cell Type ◽  
Cell Type Specificity ◽  
Splicing Speckles ◽  
Polycomb Bodies

Abstract We describe here phase-separated subnuclear organelles in the nematode Caenorhabditis elegans, which we term NUN (NUclear Nervous system-specific) bodies. Unlike other previously described subnuclear organelles, NUN bodies are highly cell type specific. In fully mature animals, 4–10 NUN bodies are observed exclusively in the nucleus of neuronal, glial and neuron-like cells, but not in other somatic cell types. Based on co-localization and genetic loss of function studies, NUN bodies are not related to other previously described subnuclear organelles, such as nucleoli, splicing speckles, paraspeckles, Polycomb bodies, promyelocytic leukemia bodies, gems, stress-induced nuclear bodies, or clastosomes. NUN bodies form immediately after cell cycle exit, before other signs of overt neuronal differentiation and are unaffected by the genetic elimination of transcription factors that control many other aspects of neuronal identity. In one unusual neuron class, the canal-associated neurons, NUN bodies remodel during larval development, and this remodeling depends on the Prd-type homeobox gene ceh-10. In conclusion, we have characterized here a novel subnuclear organelle whose cell type specificity poses the intriguing question of what biochemical process in the nucleus makes all nervous system-associated cells different from cells outside the nervous system.

scholarly journals KNOX HOMOLOGS SHOOT MERISTEMLESS (STM) and KNAT6 are epistatic to CLAVATA3 (CLV3) during embryonic meristem development in Arabidopsis thaliana

2020 ◽  
Author(s):  
Sharma Nidhi ◽  
Liu Tie
Keyword(s):  
Arabidopsis Thaliana ◽  
Shoot Apex ◽  
Double Mutant ◽  
Genetic Interaction ◽  
Homeobox Gene ◽  
The Other ◽  
Shoot Meristem ◽  
Published Data ◽  
Meristem Development ◽  
Shoot Meristemless

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.

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.

Specification of the anterior hindbrain and establishment of a normal mid/hindbrain organizer is dependent on Gbx2 gene function

Development ◽  
1997 ◽  
Vol 124 (15) ◽  
pp. 2923-2934 ◽  
Author(s):  
K.M. Wassarman ◽  
M. Lewandoski ◽  
K. Campbell ◽  
A.L. Joyner ◽  
J.L. Rubenstein ◽  
...  
Keyword(s):  
Normal Development ◽  
Motor Nerve ◽  
Homeobox Gene ◽  
Neural Plate ◽  
Mouse Embryos ◽  
Loss Of Function ◽  
Isthmic Nuclei ◽  
Signaling Center ◽  
Derivatives Of ◽  
Anterior Posterior

Analysis of mouse embryos homozygous for a loss-of-function allele of Gbx2 demonstrates that this homeobox gene is required for normal development of the mid/hindbrain region. Gbx2 function appears to be necessary at the neural plate stage for the correct specification and normal proliferation or survival of anterior hindbrain precursors. It is also required to maintain normal patterns of expression at the mid/hindbrain boundary of Fgf8 and Wnt1, genes that encode signaling molecules thought to be key components of the mid/hindbrain (isthmic) organizer. In the absence of Gbx2 function, isthmic nuclei, the cerebellum, motor nerve V, and other derivatives of rhombomeres 1–3 fail to form. Additionally, the posterior midbrain in the mutant embryos appears to be extended caudally and displays abnormalities in anterior/posterior patterning. The failure of anterior hindbrain development is presumably due to the loss of Gbx2 function in the precursors of the anterior hindbrain. However, since Gbx2 expression is not detected in the midbrain it seems likely that the defects in midbrain anterior/posterior patterning result from an abnormal isthmic signaling center. These data provide genetic evidence for a link between patterning of the anterior hindbrain and the establishment of the mid/hindbrain organizer, and identify Gbx2 as a gene required for these processes to occur normally.

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