scholarly journals Tissue specific effects of ommochrome pathway mutations in Drosophila melanogaster

1991 ◽  
Vol 57 (3) ◽  
pp. 257-266 ◽  
Author(s):  
Rick Tearle

SummaryThe tissue-specific effects of 17 mutations affecting the synthesis of brown eye pigment (xanthommatin) have been investigated by combining them with chocolate and red cells, two mutations causing ectopic pigmentation of the Malpighian tubules and larval fat body (which normally only synthesize pigment precursors). The majority of mutations block the pigmentation of four organs: the normally pigmented eyes and ocelli, and ectopically pigmented tubules and fat body. They represent genes that would appear to be required for the normal operation of the pathway per se and are likely to encode structural proteins. Mutations at 5 loci affect pigmentation of a subset of organs: cd and po affect only the eyes and ocelli; kar affects the eyes, ocelli and fat body; car causes excretion of pigment from tubules; and z affects pigmentation of the eyes alone. Of these loci, only z has been shown to encode a regulatory protein and the role of the remaining four gene products is not clear. Two mutations affecting the red eye pigments (drosopterins), bw and mal, do not substantially perturb brown pigment synthesis in any of the four organs.

1996 ◽  
Vol 16 (11) ◽  
pp. 6542-6552 ◽  
Author(s):  
E B Dubrovsky ◽  
G Dretzen ◽  
E M Berger

The steroid hormone ecdysone causes dramatic changes in the genetic programs leading to the pupariation of Drosophila melanogaster, and the Broad-Complex (BR-C) gene is known to play a key role in this process. Previously we showed that BR-C regulates developmental changes in transcription and chromatin structure of the 67B heat shock gene cluster, which contains four small hsp genes. Importantly, the downregulation of the hsp23 gene in the BR-C mutants correlates with the absence of a DNase I-hypersensitive site (DHS) at position -1400. To study the functional importance of the DHS-1400, we have introduced genomic fragments containing a modified hsp23 gene into the Drosophila germ line. Our analysis shows that the ecdysone response element is necessary but not sufficient for full developmental expression of hsp23 in the late third instar and that there is, indeed, another regulatory element, in the vicinity of DHS-1400. We also show that hsp23 developmental expression is not tissue specific. A construct lacking the ecdysone response element is unable to direct normal hsp23 expression in all tissues except the brain. Similarly, brain-specific expression is BR-C independent, although in the other tissues we find different requirements for BR-C genetic functions. The effect of the br mutations is restricted to wing imaginal discs and midgut tissue, while that of 2Bc is restricted to the fat body and Malpighian tubules, and mutations in the rbp group have no effect in any of the tissues studied. Thus, BR-C regulatory action is mediated through different genetic functions in a tissue-specific manner.


2020 ◽  
Vol 505 ◽  
pp. 110741 ◽  
Author(s):  
Coralie Fontaine ◽  
Melissa Buscato ◽  
Alexia Vinel ◽  
Frank Giton ◽  
Isabelle Raymond-Letron ◽  
...  

2008 ◽  
Vol 41 (6) ◽  
pp. 405-413 ◽  
Author(s):  
Jyotsna B Pippal ◽  
Peter J Fuller

The signature action of aldosterone in the regulation of electrolyte and fluid balance is well established. However, the role of aldosterone as an important contributor to morbidity and mortality in heart failure has gained a heightened interest in recent years, but the mechanisms of this action are not well understood. Aldosterone is the principal physiological ligand for the mineralocorticoid receptor (MR), a ligand-activated transcription factor, that also binds to the physiological glucocorticoid, cortisol. Both classes of hormones bind with similar affinity to the MR, but the molecular basis of selective and tissue-specific effects of MR ligands is not yet fully documented. The structural and functional determinants of MR function are described and their significance is discussed.


Genetics ◽  
1991 ◽  
Vol 127 (1) ◽  
pp. 151-159 ◽  
Author(s):  
S Liu ◽  
E McLeod ◽  
J Jack

Abstract The cut gene in Drosophila is necessary in at least one cell type, the external sensory organs, for proper cell type specification and morphogenesis. It is also expressed in a variety of other tissues, where its function is less well characterized. Previous work has demonstrated that mutations affecting all the tissues map in the transcribed and translated portion of the gene, while mutations that are tissue specific in their effects map in the 140 kb upstream of the most 5' exon known. Within that 140 kb, the mutations fall into four subregions, two of which contain mutations affecting unique sets of tissues and the other two of which contain mutations that affect a third set. Our examination of the defects of mutants, their complementation behavior, and their effect on the distribution of the cut protein in embryos, alters the picture in three important ways. First, some mutations convert the cells of the Malpighian tubules into what appear to be gut cells, suggesting that cut is necessary for cell type specification and morphogenesis in a variety of tissues. Second, mutations in each of the four subregions in the 140 kb of upstream DNA cause a different set of phenotypes, suggesting that the regulatory region contains at least four separate units with different tissue specific functions. And third, mutations have now been identified that map in the transcribed and translated portion of the gene but that have tissue specific effects.


Genetics ◽  
1984 ◽  
Vol 108 (4) ◽  
pp. 953-968
Author(s):  
S H Clark ◽  
S Daniels ◽  
C A Rushlow ◽  
A J Hilliker ◽  
A Chovnick

ABSTRACT Prior reports from this laboratory have described the experimental basis for our understanding of the genetic organization of the rosy locus (ry:3-52.0) of Drosophila melanogaster, as a bipartite genetic entity consisting of a structural element that codes for the xanthine dehydrogenase (XDH) peptide and a contiguous, cis-acting control element. The present report describes our progress in the analysis of the control element and its variants. Characterization of the control element variants reveals that, with respect to late third instar larval tissue distribution of XDH activity and cross-reacting material, i409H is associated with a large, tissue-specific increase in fat body which is not observed in malpighian tubules. Further data are presented in support of the inference that this differential expression must reflect differential production of XDH-specific RNA transcripts.—Gel blot analyses are described which demonstrate (1) that the phenotypic effects associated with variation in the rosy locus control element relate to differences in accumulation of XDH-specific poly-A+ RNA and (2) do not relate to differences in rosy DNA template numbers.—Experiments are described that provide for unambiguous mapping of control element sites through the use of half-tetrad recombination experiments and the recovery and phenotypic characterization of the reciprocal products of exchange between control element site variants. Thus, we are able to order the sites as follows: kar-i1005 i409-ry.


2001 ◽  
Vol 114 (7) ◽  
pp. 1321-1329 ◽  
Author(s):  
IM van Den Nieuwenhof ◽  
C. Renardel De Lavalette ◽  
N. Diaz ◽  
I. van Die ◽  
TK van Den Berg

Signal regulatory protein-(α) (SIRP(α)) is a member of the Ig superfamily selectively expressed by neuronal and myeloid cells. The molecule mediates functional interactions with CD47/integrin-associated protein. Here we provide evidence for the tissue-specific glycosylation of neuronal and haematopoietic SIRP(α). We demonstrate a major difference in the galactosylation of N-linked glycans isolated from neuronal (i.e. brain-derived) SIRP(α) as compared to myeloid (i.e. spleen-derived) SIRP(α), with neuronal SIRP(α) almost completely lacking galactose. (β)4-galactosyltransferase assays demonstrated that this is most likely due to a low galactosylation capacity of the brain. In order to investigate the role of galactosylation of SIRP(α) in cellular interactions, soluble recombinant SIRP(α) glycoforms containing galactose (SIRP(α)-Fc) or lacking galactose (SIRP(α)((Δ)Gal)-Fc) were produced. Binding studies demonstrated superior binding of SIRP(α)((Δ)Gal)-Fc to cerebellar neurons and isolated lymphocytes. In contrast, SIRP(α)-Fc bound relatively strong to macrophages. These data show that the galactosylation of SIRP(α) determines its cellular binding specificity.


2012 ◽  
Vol 52 (5) ◽  
pp. 1091-1095 ◽  
Author(s):  
Abdallah Gharib ◽  
Damien De Paulis ◽  
Bo Li ◽  
Lionel Augeul ◽  
Elisabeth Couture-Lepetit ◽  
...  

2019 ◽  
Author(s):  
Sebastian Duncan ◽  
Samuel Delage ◽  
Alexa Chioran ◽  
Olga Sirbu ◽  
Theodore J. Brown ◽  
...  

AbstractThe assembly of basement membranes (BMs) into tissue-specific morphoregulatory structures requires non-core BM components. Work in Drosophila indicates a principal role of collagen-binding matricellular glycoprotein SPARC (Secreted Protein, Acidic, Rich in Cysteine) in larval fat body BM assembly. We report that SPARC and collagen IV (Col(IV)) first colocalize in the trans-Golgi of hemocytes. Mutating the collagen-binding epitopes of SPARC leads to 2nd instar larval lethality, indicating that SPARC binding to Col(IV) is essential for survival. Analysis of this mutant reveals increased Col(IV) puncta within adipocytes and intense perimeter Col(IV) staining surrounding the fat body as compared to wild-type larvae, reflecting a disruption in chaperone-like activity. In addition, Col(IV) in the wing imaginal disc was absent. Removal of the disulfide bridge in EF-hand2, which is known to enhance Col(IV) binding by SPARC, did not lead to larval lethality; however, a similar but less intense fat body phenotype was observed. Additionally, both SPARC mutants have altered fat body BM pore topography. Wing imaginal disc-derived SPARC did not localize within Col(IV)-rich matrices, indicating a distinct variant. Collectively, these data demonstrate the essential role of Col(IV) chaperone-like activity of SPARC to Drosophila development and indicate tissue-specific variants with differential functions.


2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Jay C. Brown

This study was carried out to pursue the observation that the level of gene expression is affected by gene length in the human genome. As transcription is a time-dependent process, it is expected that gene expression will be inversely related to gene length, and this is found to be the case. Here, I describe the results of studies performed to test whether the gene length/gene expression linkage is affected by two factors, the chromosome where the gene is located and the tissue where it is expressed. Studies were performed with a database of 3538 human genes that were divided into short, midlength, and long groups. Chromosome groups were then compared in the expression level of genes with the same length. A similar analysis was performed with 19 human tissues. Tissue-specific groups were compared in the expression level of genes with the same length. Both chromosome and tissue studies revealed new information about the role of gene length in control of gene expression. Chromosome studies led to the identification of two chromosome populations that differ in the expression level of short genes. A high level of expression was observed in chromosomes 2-10, 12-15, and 18 and a low level in 1, 11, 16-17, 19-20, 22, and 24. Studies with tissue-specific genes led to the identification of two tissues, brain and liver, which differ in the expression level of short genes. The results are interpreted to support the view that the level of a gene’s expression can be affected by the chromosome and the tissue where the gene is transcribed.


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