PubMed Health⌕ Search

Biomedical subjects

T Jack

Publications and source records attributed to T Jack.

At least 19 recordsLinked to original sources
PubMed2001

Relearning our ABCs: new twists on an old model.

Over the past decade, the ABC model of flower development has been widely promulgated. However, correct flower-organ development requires not only the ABC genes but also the SEPALLATA genes. When the SEPALLATA genes are expressed together with the ABC genes, both vegetative and cauline leaves are converted to floral organs. Most of the ABC genes and all three SEPALLATA genes encode MADS transcription factors, which bind to DNA as dimers. Here, amendments to the ABC model are considered that incorporate both the SEPALLATA genes and the ability of MADS proteins to form higher-order complexes.

ATP-Binding Cassette Transporters↗
PubMed2001

Plant development going MADS.

It has been known for a decade that the plant MADS genes are important regulators of meristem and floral organ identity. The MADS family in Arabidopsis consists of more than 80 members and, until recently, the function of the majority of these genes was unknown. With the enhanced ability to generate loss-of-function mutants and overexpression lines, the function of the MADS gene family members is beginning to be elucidated. Recent progress demonstrates that MADS genes in Arabidopsis are important regulators not only of meristem and floral organ identity but also of flowering timing and cell-type specification in floral organs.

Arabidopsis↗
PubMed2000

An enhancer trap line associated with a D-class cyclin gene in Arabidopsis.

In yeast and animals, cyclins have been demonstrated to be important regulators of cell cycle progression. In recent years, a large number of A-, B-, and D-class cyclins have been isolated from a variety of plant species. One class of cyclins, the D-class cyclins, is important for progression through G1 phase of the cell cycle. In Arabidopsis, four D-class cyclins have been isolated and characterized (CYCLIN-D1;1, CYCLIN-D2;1, CYCLIN-D3;1, and CYCLIN-D4;1). In this report we describe the characterization of a fifth D-class cyclin gene, CYCLIN-D3;2 (CYCD3;2), from Arabidopsis. An enhancer trap line, line 5580, contains a T-DNA insertion in CYCD3;2. Enhancer trap line 5580 exhibits expression in young vegetative and floral primordia. In line 5580, T-DNA is inserted in the first exon of the CYCD3;2 gene; in homozygous 5580 plants CYCD3;2 RNA is not detectable. Even though CYCD3;2 gene function is eliminated, homozygous 5580 plants do not exhibit an obvious growth or developmental phenotype. Via in situ hybridization we demonstrate that CYCD3;2 RNA is expressed in developing vegetative and floral primordia. In addition, CYCD3;2 is also capable of rescuing a yeast strain that is deficient in G1 cyclin activity.

Amino Acid Sequence↗
PubMed1999

Generation of enhancer trap lines in Arabidopsis and characterization of expression patterns in the inflorescence.

Eleven thousand, three hundred and seventy enhancer/promoter trap lines in Arabidopsis were generated via T-DNA transformation utilizing the binary vector pD991 that contains a minimal promoter fused to the uidA reporter gene. Overall 31% of the lines generated exhibit a staining pattern in the inflorescence. Flanking DNA has been cloned from 15 lines exhibiting inflorescence staining patterns by either thermal asymmetric interlaced PCR (TAIL-PCR), inverse PCR (IPCR), or partial library construction. Seeds from these lines are available from the ABRC and NASC Arabidopsis stock centers and DNA pools are available from the ABRC.

Arabidopsis↗
PubMed1998

A leak of concern.

Explore the source record for details and available documents.

Anesthesia, Closed-Circuit↗
PubMed1998

An intragenic suppressor of the Arabidopsis floral organ identity mutant apetala3-1 functions by suppressing defects in splicing.

The Arabidopsis floral organ identity gene APETALA3 (AP3) specifies the identity of petals and stamens in the flower. In flowers mutant for the temperature-sensitive ap3-1 allele, the petals and stamens are partially converted to sepals and carpels, respectively. ap3-1 contains a single nucleotide change in the AP3 gene that alters both an amino acid in the AP3 protein and the 5' splice consensus site for intron 5. Surprisingly, the Ap3-1 mutant phenotype is not due to the missense mutation but instead is due to defects in splicing; specifically, exon 5 is frequently skipped by the splicing machinery at the restrictive temperature. In a screen for suppressors of ap3-1, we isolated an intragenic suppressor, ap3-11, that functions to suppress the splicing defects of ap3-1. Using a reverse transcriptase-polymerase chain reaction assay, we demonstrate that the percentage of full-length exon 5-containing AP3 RNAs correlates with the phenotype of the flowers in both ap3-1 and ap3-11. Rather surprisingly, the ap3-11 suppressor mutation is located in intron 4. One model explaining the function of ap3-11 is that the ap3-11 suppressor creates a novel branch point sequence that causes exon 5 to be more frequently recognized by the splicing machinery. The identification of such a suppressor strongly suggests that exon-scanning models of intron-exon recognition are operative in plants.

Arabidopsis↗
PubMed1998

The CArG boxes in the promoter of the Arabidopsis floral organ identity gene APETALA3 mediate diverse regulatory effects.

APETALA3 is a MADS box gene required for normal development of the petals and stamens in the Arabidopsis flower. Studies in yeast, mammals and plants demonstrate that MADS domain transcription factors bind with high affinity to a consensus sequence called the CArG box. The APETALA3 promoter contains three close matches to the consensus CArG box sequence. To gain insights into the APETALA3 regulatory circuitry, we have analyzed the APETALA3 promoter using AP3::uidA(GUS) fusions. 496 base pairs of APETALA3 promoter sequence 5' to the transcriptional start directs GUS activity in the same temporal and spatial expression pattern as the APETALA3 RNA and protein in wild-type flowers. A synthetic promoter consisting of three tandem repeats of a 143 base pair sequence directs reporter gene activity exclusively to petals and stamens in the flower. We have analyzed the role of the CArG boxes by site-specific mutagenesis and find that the three CArG boxes mediate discrete regulatory effects. Mutations in CArG1 result in a decrease in reporter expression suggesting that CArG1 is the binding site for a positively acting factor or factors. Mutations in CArG2 result in a decrease in reporter expression in petals, but the expression pattern in stamens is unchanged. By contrast, mutations in CArG3 result in an increase in the level of reporter gene activity during early floral stages suggesting that CArG3 is the binding site for a negatively acting factor.

Arabidopsis↗
PubMed1997

Targeted misexpression of AGAMOUS in whorl 2 of Arabidopsis flowers.

In Arabidopsis, transcripts of the floral organ identity genes APETALA3, APETALA1, AGAMOUS, and PISTILLATA are expressed only in a subset of the floral organs. To test and extend present models for establishment of floral organ identity, we constructed a transgenic line that expresses the AGAMOUS gene under the control of the APETALA3 promotor (pAP3::AG). In wild-type flowers, AGAMOUS is expressed in the third and fourth floral whorls, whereas APETALA3 is expressed at high levels in whorls two and three. Under the control of the APETALA3 promotor, AGAMOUS is misexpressed in the second whorl of the flower. The organs in the second whorl of pAP3::AG flowers either fail to develop or develop as stamens. When pAP3::AG is crossed to the homeotic mutants apetala1, apetala3, pistilla, agamous and superman, novel floral phenotypes result. In pAP3::AG agamous-3 mutants, the flowers are indeterminate and consist of a repetition of sepals and stamens, rather that sepals and petals, as is observed in agamous single mutants; the indeterminacy demonstrates that AG is required in the fourth whorl to make a flower determinate.

AGAMOUS Protein, Arabidopsis↗
PubMed1994

Arabidopsis homeotic gene APETALA3 ectopic expression: transcriptional and posttranscriptional regulation determine floral organ identity.

APETALA3 (AP3) specifies the development of petals and stamens in the Arabidopsis flower. We constructed a transgenic line, 35S-AP3, that ectopically expresses AP3 under the control of a constitutive promoter. The resulting flowers exhibit a replacement of carpels by stamens and resemble flowers homozygous for the previously described Arabidopsis mutation superman. Although AP3 RNA is detected at high levels throughout the flower and stem in 35S-AP3, AP3 protein is detected at high levels only in the second, third, and fourth floral whorls, demonstrating that AP3 is posttranscriptionally regulated. Ectopic expression of AP3 causes a second floral homeotic gene, PISTILLATA (PI), to function in the fourth whorl of 35S-AP3 flowers. AP3 and PI also activate an AP3 promoter-reporter gene fusion, demonstrating that AP3 positively autoregulates.

Arabidopsis↗
PubMed1992

The homeotic gene APETALA3 of Arabidopsis thaliana encodes a MADS box and is expressed in petals and stamens.

Mutations in the APETALA3 (AP3) gene of A. thaliana result in homeotic transformations of petals to sepals and stamens to carpels. We have cloned the AP3 gene from Arabidopsis based on its homology to the homeotic flower gene deficiens (DEFA) from the distantly related plant Antirrhinum majus. The sequence of four ap3 mutant alleles and genetic mapping analysis prove that the DEFA homolog is AP3. Like several other plant homeotic genes, the AP3 gene contains a MADS box and likely acts as a transcription factor. The region-specific spatial expression pattern of AP3 rules out certain types of sequential models of flower development and argues in favor of a spatial model based on positional information. Since DEFA and AP3 have very similar protein products, mutant phenotypes, and spatial expression patterns, it is likely that these genes are cognate homologs.

Alleles↗
PubMed1992

SUPERMAN, a regulator of floral homeotic genes in Arabidopsis.

We describe a locus, SUPERMAN, mutations in which result in extra stamens developing at the expense of the central carpels in the Arabidopsis thaliana flower. The development of superman flowers, from initial primordium to mature flower, is described by scanning electron microscopy. The development of doubly and triply mutant strains, constructed with superman alleles and previously identified homeotic mutations that cause alterations in floral organ identity, is also described. Essentially additive phenotypes are observed in superman agamous and superman apetala2 double mutants. The epistatic relationships observed between either apetala3 or pistillata and superman alleles suggest that the SUPERMAN gene product could be a regulator of these floral homeotic genes. To test this, the expression patterns of AGAMOUS and APETALA3 were examined in superman flowers. In wild-type flowers, APETALA3 expression is restricted to the second and third whorls where it is required for the specification of petals and stamens. In contrast, in superman flowers, APETALA3 expression expands to include most of the cells that would normally constitute the fourth whorl. This ectopic APETALA3 expression is proposed to be one of the causes of the development of the extra stamens in superman flowers. The spatial pattern of AGAMOUS expression remains unaltered in superman flowers as compared to wild-type flowers. Taken together these data indicate that one of the functions of the wild-type SUPERMAN gene product is to negatively regulate APETALA3 in the fourth whorl of the flower. In addition, superman mutants exhibit a loss of determinacy of the floral meristem, an effect that appears to be mediated by the APETALA3 and PISTILLATA gene products.

Gene Expression Regulation↗
PubMed1991

Reticulum cell sarcoma: two complete 'spontaneous' regressions, in response to high-dose ascorbic acid therapy. A report on subsequent progress.

In 1975, we reported the remarkable case of a 42-year-old man with histologically proven widely disseminated reticulum cell sarcoma who, in a remarkably short time, appeared to enjoy not one, but two, complete spontaneous regressions of his fatal illness. Both these regressions coincided exactly in time with intravenous high-dose ascorbate administration, and it seemed reasonable to conclude that this unconventional therapy must have been responsible for his excellent responses. For those interested in spontaneous regressions of cancer and the possible mechanisms, we now report his subsequent progress some 17 years later.

Adenocarcinoma↗
PubMed1991

A genetic and molecular model for flower development in Arabidopsis thaliana.

Cells in developing organisms do not only differentiate, they differentiate in defined patterns. A striking example is the differentiation of flowers, which in most plant families consist of four types of organs: sepals, petals, stamens and carpels, each composed of characteristic cell types. In the families of flowering plants in which these organs occur, they are patterned with the sepals in the outermost whorl or whorls of the flower, with the petals next closest to the center, the stamens even closer to the center, and the carpels central. In each species of flowering plant the disposition and number (or range of numbers) of these organs is also specified, and the floral 'formula' is repeated in each of the flowers on each individual plant of the species. We do not know how cells in developing plants determine their position, and in response to this determination differentiate to the cell types appropriate for that position. While there have been a number of speculative proposals for the mechanism of organ specification in flowers (Goethe, 1790; Goebel, 1900; Heslop-Harrison, 1964; Green, 1988), recent genetic evidence is inconsistent with all of them, at least in the forms in which they were originally presented (Bowman et al. 1989; Meyerowitz et al. 1989). We describe here a preliminary model, based on experiments with Arabidopsis thaliana. The model is by and large consistent with existing evidence, and has predicted the results of a number of genetic and molecular experiments that have been recently performed.

Models, Chemical↗
PubMed1990

Establishment of the Deformed expression stripe requires the combinatorial action of coordinate, gap and pair-rule proteins.

In Drosophila embryos, anterior-posterior positional identities are set and maintained by the expression boundaries of homeotic selector genes. The establishment of the initial expression boundaries of the homeotic genes are in turn dependent on earlier acting patterning genes of Drosophila. To define the combinations of early genes that are required to establish a unique blastoderm stripe of expression of the homeotic gene Deformed, we have analysed single and double patterning mutants and heat shock promoter fusion constructs that ectopically express early acting regulators. We find that the activation of Deformed is dependent on combinatorial input from at least three levels of the early hierarchy. The simplest activation code sufficient to establish Deformed expression, given the absence of negative regulators such as fushi-tarazu, consists of a moderate level of expression from the coordinate gene bicoid, in combination with expression from both the gap gene hunchback, and the pair-rule gene even-skipped. In addition, the activation code for Deformed is redundant; other pair-rule genes in addition to even-skipped can apparently act in combination with bicoid and hunchback to activate Deformed.

Alleles↗
PubMed1990

Ectopic expression from the Deformed gene triggers a dominant defect in Drosophila adult head development.

Drosophila adults carrying a dominant allele of the Deformed locus (DfdD) have a mutant phenotype in which lower eye and orbital structures of the adult head are eliminated. The molecular defect responsible for this dominant mutation is a large, transposon-flanked, fragment of DNA inserted downstream of the Deformed (Dfd) transcription unit. The downstream transposon-flanked insert causes the inappropriate activation of Dfd gene expression in a subset of the cells of the eye imaginal disc, resulting in their abnormal development, and in the loss of lower eye structures from the adult head. A chromosome selected for its reversion of the dominant phenotype is missing a portion of the transposon-flanked insert and reverts to a normal expression pattern of Dfd in the eye-antennal disc. Additional evidence that the dominant head phenotype is caused by ectopic expression of Dfd in the eye disc derives from experiments showing that a DfdD-like phenotype can be induced by ectopic expression of a Dfd gene under heat shock promoter control.

Animals↗