Effect of GA 3 and paclobutrazol on adventitious shoot regeneration of two Pelargonium sp

This study had two aims. The first was to improve the regeneration efficiency of Pelargonium leaf discs by adventitious budding. The second was to test the effect of gibberellic acid (GA 3) and paclobutrazol (PBZ) on callus formation and adventitious shoot regeneration in Pelargonium before using genetic transformation of this species for functional validation of genes involved in the process of GA regulation. GA 3 and paclobutrazol (an inhibitor of GA synthesis pathway) were added (together or separately) in the shoot regeneration media of two Pelargonium species, Pelargonium * hortorum \u27Panache sud\u27 (\u27P.sud\u27) and Pelargonium * domesticum \u27Autumn haze\u27 (\u27 P.dom\u27). In both cases, GA 3 applied alone, completely inhibited the bud regeneration. Moreover, the rate of callus formation decreased drastically when 5 M of GA 3 was applied to \u27 P. dom\u27 explants. Similar result was obtained with \u27P.sud\u27 explants using 20 M GA 3. Paclobutrazol (0.3 M) applied at the same time as GA 3 (10 M) could partially restore regeneration process of \u27 P. dom\u27. For \u27 P. dom\u27, the use of paclobutrazol alone increased callus formation and slightly improved the rate of regeneration. Moreover, initiated buds had a better appearance. For \u27P. sud\u27, which had an abundant callusing, paclobutrazol did not improve regeneration and led to hyperhydric shoots

Mutation analysis of the Fanconi anaemia A gene in breast tumours with loss of heterozygosity at 16q24.3

The recently identified Fanconi anaemia A (FAA) gene is located on chromosomal band 16q24.3 within a region that has been frequently reported to show loss of heterozygosity (LOH) in breast cancer. FAA mutation analysis of 19 breast tumours with specific LOH at 16q24.3 was performed. Single-stranded conformational polymorphism (SSCP) analysis on cDNA and genomic DNA, and Southern blotting failed to identify any tumour-specific mutations. Five polymorphisms were identified, but frequencies of occurrence did not deviate from those in a normal control population. Therefore, the FAA gene is not the gene targeted by LOH at 16q24.3 in breast cancer. Another tumour suppressor gene in this chromosomal region remains to be identified. © 1999 Cancer Research Campaig

Early childhood pedagogies: spaces for young children to flourish

This paper introduces the Special Issue of Early Child Development and Care focused on Early Childhood Pedagogy. It opens by considering past and present discourses concerning early childhood pedagogy, and focus is given to established philosophical underpinnings in the field and their translation to contemporary guidance, alongside research and policy. It is argued that early childhood pedagogy is a contested, complex and diverse space, yet these factors are entirely appropriate for supporting young children to flourish as valued individuals in different contexts. Building on this argument, it is posited that it may be more appropriate to discuss early childhood pedagogies rather than early childhood pedagogy. The paper goes on to critique a range of established early childhood pedagogies, before introducing 18 papers from across the world that make exciting new contributions to the discourse. It is intended that this collection will inspire new debates and fresh endeavours concerning early childhood pedagogies

Analysis of the 10q23 chromosomal region and the PTEN gene in human sporadic breast carcinoma

We examined a panel of sporadic breast carcinomas for loss of heterozygosity (LOH) in a 10-cM interval on chromosome 10 known to encompass the PTEN gene. We detected allele loss in 27 of 70 breast tumour DNAs. Fifteen of these showed loss limited to a subregion of the area studied. The most commonly deleted region was flanked by D10S215 and D10S541 and encompasses the PTEN locus. We used a combination of denaturing gradient gel electrophoresis and single-strand conformation polymorphism analyses to investigate the presence of PTEN mutations in tumours with LOH in this region. We did not detect mutations of PTEN in any of these tumours. Our data show that, in sporadic breast carcinoma, loss of heterozygosity of the PTEN locus is frequent, but mutation of PTEN is not. These results are consistent with loss of another unidentified tumour suppressor in this region in sporadic breast carcinoma. © 1999 Cancer Research Campaig

The cystic fibrosis transmembrane recruiter the alter ego of CFTR as a multi-kinase anchor

This review focuses on a newly discovered interaction between protein kinases involved in cellular energetics, a process that may be disturbed in cystic fibrosis for unknown reasons. I propose a new model where kinase-mediated cellular transmission of energy provides mechanistic insight to a latent role of the cystic fibrosis transmembrane conductance regulator (CFTR). I suggest that CFTR acts as a multi-kinase recruiter to the apical epithelial membrane. My group finds that, in the cytosol, two protein kinases involved in cell energy homeostasis, nucleoside diphosphate kinase (NDPK) and AMP-activated kinase (AMPK), bind one another. Preliminary data suggest that both can also bind CFTR (function unclear). The disrupted role of this CFTR-kinase complex as ‘membrane transmitter to the cell’ is proposed as an alternative paradigm to the conventional ion transport mediated and CFTR/chloride-centric view of cystic fibrosis pathogenesis. Chloride remains important, but instead, chloride-induced control of the phosphohistidine content of one kinase component (NDPK, via a multi-kinase complex that also includes a third kinase, CK2; formerly casein kinase 2). I suggest that this complex provides the necessary near-equilibrium conditions needed for efficient transmission of phosphate energy to proteins controlling cellular energetics. Crucially, a new role for CFTR as a kinase controller is proposed with ionic concentration acting as a signal. The model posits a regulatory control relay for energy sensing involving a cascade of protein kinases bound to CFTR

Developmental malformation of the corpus callosum: a review of typical callosal development and examples of developmental disorders with callosal involvement

This review provides an overview of the involvement of the corpus callosum (CC) in a variety of developmental disorders that are currently defined exclusively by genetics, developmental insult, and/or behavior. I begin with a general review of CC development, connectivity, and function, followed by discussion of the research methods typically utilized to study the callosum. The bulk of the review concentrates on specific developmental disorders, beginning with agenesis of the corpus callosum (AgCC)—the only condition diagnosed exclusively by callosal anatomy. This is followed by a review of several genetic disorders that commonly result in social impairments and/or psychopathology similar to AgCC (neurofibromatosis-1, Turner syndrome, 22q11.2 deletion syndrome, Williams yndrome, and fragile X) and two forms of prenatal injury (premature birth, fetal alcohol syndrome) known to impact callosal development. Finally, I examine callosal involvement in several common developmental disorders defined exclusively by behavioral patterns (developmental language delay, dyslexia, attention-deficit hyperactive disorder, autism spectrum disorders, and Tourette syndrome)