Genetic regulation of tissue-specific expression of amylase structural genes in Drosophila melanogaster.
(17/18964)
Laboratory strains of Drosophila melanogaster were screened for spatial variations in adult midgut alpha-amylase (1,4-alpha-D-glucan glucanohydrolase, EC 3.2.1.1) expression. No strain-specific differences were found anteriorly, but three patterns of activity were discerned in the posterior midgut: A, activity throughout most of the region; B, activity in the anterior part of the region; and C, little or no activity. Alleles of a control gene, map, are responsible for this tissue-specific regulation of activity; e.g., mapA homozygotes produce the A pattern and mapC homozygotes the C pattern. The map locus was placed at 2--80 +/- on the genetic map of chromosome 2R, about two crossover units distal to the Amy structural gene region for alpha-amylase. Electrophoretic studies showed that mapA is trans acting in mapA/mapC flies, allowing expression of amylase isozymes coded for by genes on the opposite chromosome. The map gene behaves as a temporal gene that is clearly separable from the tightly linked, duplicated Amy structural genes. (+info)
Assignment of genes for immunoglobulin kappa and heavy chains to chromosomes 6 and 12 in mouse.
(18/18964)
Using somatic cell hybrids from fusions of lymphocytes of two different mouse stocks with the myeloma cell line X63-Ag8, we have assigned genes for the immunoglobulin heavy and kappa-type light chains to chromosomes 12 and 6, respectively. The two mouse stocks exhibit karyotypes consisting of nine pairs of metacentric chromosomes as a result of centric fusions of acrocentric chromosomes in different combinations. In the hybrid cells these metacentric chromosomes can be distinguished from the acrocentric chromosomes of myeloma origin, permitting correlation of Ig chain expression with mitotic loss of individual metacentric chromosomes. (+info)
TargetFinder: searching annotated sequence databases for target genes of transcription factors.
(19/18964)
TargetFinder is a new software tool to search a database of annotated sequences for transcription factor binding sites located in context with other important transcription regulatory signals and regions, like the TATA element, the promoter, and so on, thereby greatly reducing the background usually associated with this kind of search. AVAILABILITY: The TargetFinder Web service is available at http://hercules.tigem.it/TargetFinder.html CONTACT: [email protected] (+info)
ERGIC-53 gene structure and mutation analysis in 19 combined factors V and VIII deficiency families.
(20/18964)
Combined factors V and VIII deficiency is an autosomal recessive bleeding disorder associated with plasma levels of coagulation factors V and VIII approximately 5% to 30% of normal. The disease gene was recently identified as the endoplasmic reticulum-Golgi intermediate compartment protein ERGIC-53 by positional cloning, with the detection of two founder mutations in 10 Jewish families. To identify mutations in additional families, the structure of the ERGIC-53 gene was determined by genomic polymerase chain reaction (PCR) and sequence analysis of bacterial artificial chromosome clones containing the ERGIC-53 gene. Nineteen additional families were analyzed by direct sequence analysis of the entire coding region and the intron/exon junctions. Seven novel mutations were identified in 10 families, with one additional family found to harbor one of the two previously described mutations. All of the identified mutations would be predicted to result in complete absence of functional ERGIC-53 protein. In 8 of 19 families, no mutation was identified. Genotyping data indicate that at least two of these families are not linked to the ERGIC-53 locus. Taken together, these results suggest that a significant subset of combined factors V and VIII deficiency is due to mutation in one or more additional genes. (+info)
Two constituents of the initiation complex of the mannan-binding lectin activation pathway of complement are encoded by a single structural gene.
(21/18964)
Mannan-binding lectin (MBL) forms a multimolecular complex with at least two MBL-associated serine proteases, MASP-1 and MASP-2. This complex initiates the MBL pathway of complement activation by binding to carbohydrate structures present on bacteria, yeast, and viruses. MASP-1 and MASP-2 are composed of modular structural motifs similar to those of the C1q-associated serine proteases C1r and C1s. Another protein of 19 kDa with the same N-terminal sequence as the 76-kDa MASP-2 protein is consistently detected as part of the MBL/MASP complex. In this study, we present the primary structure of this novel MBL-associated plasma protein of 19 kDa, MAp19, and demonstrate that MAp19 and MASP-2 are encoded by two different mRNA species generated by alternative splicing/polyadenylation from one structural gene. (+info)
Complexity in biological signaling systems.
(22/18964)
Biological signaling pathways interact with one another to form complex networks. Complexity arises from the large number of components, many with isoforms that have partially overlapping functions; from the connections among components; and from the spatial relationship between components. The origins of the complex behavior of signaling networks and analytical approaches to deal with the emergent complexity are discussed here. (+info)
Genetics of cortisone-induced cleft palate in the mouse-embryonic and maternal effects.
(23/18964)
Differences between mouse strains in frequency of embryonic, cortisone-induced cleft palate were examined. Probit analysis demonstrated a family of linear and parallel dose-response curves for different inbred and hybrid embryos. Since the differences between genotypes were not in the slopes of the response curves but rather in their location, it is proposed that the median effective dose (ED50) of cortisone required to induce cleft palate (or the tolerance) provides a more appropriate definition of the response trait and its difference that a frequency statement. The tolerance of C57BL/6J is dominant to that of A/J. A maternal effect of A/J relative to C57BL/6J dams caused a two-fold reduction in the embryonic tolerance of cortisone. Cortisone-induced cleft palate and mortality were separate response traits. In these and previous studies on cortisone- and other glucocorticoid-induced cleft palate in the mouse, the nature of the cleft-palate-response curve appeared to be the same for all glucocorticoids, and within-strain differences in tolerance could be used as measures of potency or bioassays for a particular effect of the glucocorticoids. (+info)
Gene differences between third-chromosome inversions of Drosophila pseudobscura.
(24/18964)
Associations of alleles of the acid phosphatase-3 locus with the different third-chromosome inversions from different populations of D. pseudoobscura are described. We observe only the allele AP-3(1.0) in the Standard and Arrowhead inversions and the allele AP-3.98 in the Santa Cruz, Treeline, Cuernavaca and the Pikes Peak arrangements. The Chiricahua gene arrangement is polymorphic. (+info)