scholarly journals LETHAL EFFECTS OF LOW AND "NULL" ACTIVITY ALLELES OF 6-PHOSPHOGLUCONATE DEHYDROGENASE IN DROSOPHILA MELANOGASTER

Genetics ◽  
1975 ◽  
Vol 79 (3) ◽  
pp. 451-457
Author(s):  
Glenn C Bewley ◽  
John C Lucchesi
Keyword(s):  
Drosophila Melanogaster ◽  
Embryonic Development ◽  
Enzymatic Activity ◽  
Null Allele ◽  
Developmental Rate ◽  
Lethal Effects ◽  
Homozygous Condition ◽  
Phosphogluconate Dehydrogenase ◽  
Relative Viability ◽  
Low Activity

ABSTRACT EMS-induced "null" and low activity alleles for 6-phosphogluconate dehydrogenase were characterized with respect to enzymatic activity, relative viability, fertility, and the effective lethal phase. It was determined that flies hemizygous and homozygous for the low activity allele, Pgd  -, possessed a depressed developmental rate, diminished viability, and loss of female fertility. Heterozygotes for Pgd  - and a deficiency for Pgd  + were lethal. The "null" activity allele demonstrated a lethal phenotype in both the hemizygous and homozygous condition. The effective lethal phase for the "null" allele occurs during late embryonic development (20-22 hr).

Live Confocal Analysis of Fertilization and Early Development

2001 ◽  
Vol 7 (S2) ◽  
pp. 1012-1013
Author(s):  
Uyen Tram ◽  
William Sullivan
Keyword(s):  
Drosophila Melanogaster ◽  
Embryonic Development ◽  
Real Time ◽  
Early Development ◽  
Fluorescent Probes ◽  
Primary Defect ◽  
Fluorescent Analysis ◽  
Dynamic Event ◽  
Enormous Amount ◽  
Fluorescent Studies

Embryonic development is a dynamic event and is best studied in live animals in real time. Much of our knowledge of the early events of embryogenesis, however, comes from immunofluourescent analysis of fixed embryos. While these studies provide an enormous amount of information about the organization of different structures during development, they can give only a static glimpse of a very dynamic event. More recently real-time fluorescent studies of living embryos have become much more routine and have given new insights to how different structures and organelles (chromosomes, centrosomes, cytoskeleton, etc.) are coordinately regulated. This is in large part due to the development of commercially available fluorescent probes, GFP technology, and newly developed sensitive fluorescent microscopes. For example, live confocal fluorescent analysis proved essential in determining the primary defect in mutations that disrupt early nuclear divisions in Drosophila melanogaster. For organisms in which GPF transgenics is not available, fluorescent probes that label DNA, microtubules, and actin are available for microinjection.

scholarly journals Single and mixed exposure to cadmium and mercury in Drosophila melanogaster: Molecular responses and impact on post-embryonic development

2021 ◽  
Vol 220 ◽  
pp. 112377
Author(s):  
Laëtitia Frat ◽  
Thomas Chertemps ◽  
Élise Pesce ◽  
Françoise Bozzolan ◽  
Matthieu Dacher ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Embryonic Development ◽  
Molecular Responses ◽  
Mixed Exposure

scholarly journals Genetic and Molecular Characterization of sting, a Gene Involved in Crystal Formation and Meiotic Drive in the Male Germ Line of Drosophila melanogaster

Genetics ◽  
1999 ◽  
Vol 151 (2) ◽  
pp. 749-760 ◽  
Author(s):  
Armin Schmidt ◽  
Gioacchino Palumbo ◽  
Maria P Bozzetti ◽  
Patrizia Tritto ◽  
Sergio Pimpinelli ◽  
...  
Keyword(s):  
Amino Acids ◽  
Drosophila Melanogaster ◽  
Null Allele ◽  
Germ Line ◽  
Meiotic Drive ◽  
P Element ◽  
Crystal Formation ◽  
Male Sterile ◽  
Male Sterile Mutation

Abstract The sting mutation, caused by a P element inserted into polytene region 32D, was isolated by a screen for male sterile insertions in Drosophila melanogaster. This sterility is correlated with the presence of crystals in spermatocytes and spermatids that are structurally indistinguishable from those produced in males carrying a deficiency of the Y-linked crystal (cry) locus. In addition, their morphology is needle-like in Ste+ flies and star-shaped in Ste flies, once again as observed in cry– males. The sti mutation leads to meiotic drive of the sex chromosomes, and the strength of the phenomenon is correlated with the copy number of the repetitive Ste locus. The same correlation is also true for the penetrance of the male sterile mutation. A presumptive sti null allele results in male sterility and lethal maternal effect. The gene was cloned and shown to code for a putative protein that is 866 amino acids long. A C-terminal domain of 82 amino acids is identified that is well conserved in proteins from different organisms. The gene is expressed only in the germline of both sexes. The interaction of sting with the Ste locus can also be demonstrated at the molecular level. While an unprocessed 8-kb Ste primary transcript is expressed in wild-type males, in X/Y homozygous sti males, as in X/Y cry– males, a 0.7-kb mRNA is produced.

Enzyme Activities of NADPH-Forming Metabolic Pathways in Normal and Leukemic Leukocytes

1975 ◽  
Vol 21 (7) ◽  
pp. 880-883 ◽  
Author(s):  
Francesco Belfiore ◽  
Vito Borzi ◽  
Luigi Lo Vecchio ◽  
Elena Napoli ◽  
Agata M Rabuazzo
Keyword(s):  
Malate Dehydrogenase ◽  
Metabolic Pathways ◽  
Normal Subjects ◽  
Atp Citrate Lyase ◽  
Phosphogluconate Dehydrogenase ◽  
Myelocytic Leukemia ◽  
Citrate Lyase ◽  
Enzymatic Characteristic ◽  
I Cells ◽  
Low Activity

Abstract With respect to the enzymes of NADPH-forming metabolic pathways in human leukocytes: (a) Glucose-6phosphate dehydrogenase and phosphogluconate dehydrogenase (decarboxylating) were less active in leukocytes (mostly myeloblasts) from eight patients with acute myeloblastic leukemia (I) than in leukocytes (mostly granulocytes) from 16 normal subjects (II) or 16 patients with chronic myelocytic leukemia (III). (b) Of the enzymes of the citrate cleavage pathway, ATP citrate lyase and malate dehydrogenase (decarboxylating) (NADP+) were virtually absent in the cells studied. (c) Isocitrate dehydrogenase (NADP+), aspartate aminotransferase, and alanine aminotransferase, which, together with the much more active malate dehydrogenase, constitute a newly proposed NADPH-forming metabolic cycle, showed a higher activity in I than in II or III, and therefore could compensate, as concerns NADPHgeneration, for the low activity of pentose cycle dehydrogenases. We are not sure whether the enzymatic characteristic of I cells is attributable to their immaturity or to their leukemic nature.

scholarly journals Interacting proteins identified by genetic interactions: a missense mutation in alpha-tubulin fails to complement alleles of the testis-specific beta-tubulin gene of Drosophila melanogaster.

1989 ◽  
Vol 9 (3) ◽  
pp. 875-884 ◽  
Author(s):  
T S Hays ◽  
R Deuring ◽  
B Robertson ◽  
M Prout ◽  
M T Fuller
Keyword(s):  
Drosophila Melanogaster ◽  
Missense Mutation ◽  
Null Allele ◽  
Genetic Interaction ◽  
Structural Proteins ◽  
Interacting Proteins ◽  
Tubulin Gene ◽  
Beta Tubulin ◽  
Gene Encoding ◽  
Alpha Tubulin

In this paper we demonstrate that failure to complement between mutations at separate loci can be used to identify genes that encode interacting structural proteins. A mutation (nc33) identified because it failed to complement mutant alleles of the gene encoding the testis-specific beta 2-tubulin of Drosophila melanogaster (B2t) did not map to the B2t locus. We show that this second-site noncomplementing mutation is a missense mutation in alpha-tubulin that results in substitution of methionine in place of valine at amino acid 177. Because alpha- and beta-tubulin form a heterodimer, our results suggest that the genetic interaction, failure to complement, is based on the structural interaction between the protein products of the two genes. Although the nc33 mutation failed to complement a null allele of B2t (B2tn), a deletion of the alpha-tubulin gene to which nc33 mapped complemented B2tn. Thus, the failure to complement appears to require the presence of the altered alpha-tubulin encoded by the nc33 allele, which may act as a structural poison when incorporated into either the tubulin heterodimer or microtubules.

scholarly journals The ash-1, ash-2 and trithorax genes of Drosophila melanogaster are functionally related.

Genetics ◽  
1989 ◽  
Vol 121 (3) ◽  
pp. 517-525 ◽  
Author(s):  
A Shearn
Keyword(s):  
Drosophila Melanogaster ◽  
Null Allele ◽  
Homeotic Gene ◽  
Bithorax Complex ◽  
Substantial Evidence ◽  
Genetic Tests ◽  
Recessive Lethal ◽  
The Third ◽  
Sex Combs

Abstract Mutations in the ash-1 and ash-2 genes of Drosophila melanogaster cause a wide variety of homeotic transformations that are similar to the transformations caused by mutations in the trithorax gene. Based on this similar variety of transformations, it was hypothesized that these genes are members of a functionally related set. Three genetic tests were employed here to evaluate that hypothesis. The first test was to examine interactions of ash-1, ash-2 and trithorax mutations with each other. Double and triple heterozygotes of recessive lethal alleles express characteristic homeotic transformations. For example, double heterozygotes of a null allele of ash-1 and a deletion of trithorax have partial transformations of their first and third legs to second legs and of their halteres to wings. The penetrance of these transformations is reduced by a duplication of the bithorax complex. The second test was to examine interactions with a mutation in the female sterile (1) homeotic gene. The penetrance of the homeotic phenotype in progeny from mutant mothers is increased by heterozygosis for alleles of ash-1 or ash-2 as well as for trithorax alleles. The third test was to examine the interaction with a mutation of the Polycomb gene. The extra sex combs phenotype caused by heterozygosis for a deletion of Polycomb is suppressed by heterozygosis for ash-1, ash-2 or trithorax alleles. The fact that mutations in each of the three genes gave rise to similar results in all three tests represents substantial evidence that ash-1, ash-2 and trithorax are members of a functionally related set of genes.

scholarly journals Functional cross-talk between allosteric effects of activating and inhibiting ligands underlies PKM2 regulation

2018 ◽  
Author(s):  
Jamie A. Macpherson ◽  
Alina Theisen ◽  
Laura Masino ◽  
Louise Fets ◽  
Paul C. Driscoll ◽  
...  
Keyword(s):  
Enzymatic Activity ◽  
High Activity ◽  
Pyruvate Kinase ◽  
Cross Talk ◽  
Glycolytic Enzyme ◽  
Computational Framework ◽  
Allosteric Inhibitor ◽  
Fructose 1,6 Bisphosphate ◽  
Low Activity

ABSTRACTAllosteric regulation is central to the role of the glycolytic enzyme pyruvate kinase M2 (PKM2) in cellular metabolism. Multiple activating and inhibitory allosteric ligands regulate PKM2 activity by controlling the equilibrium between high activity tetramers and low activity dimers and monomers. However, it remains elusive how allosteric inputs upon simultaneous binding of different ligands are integrated to regulate PKM2 activity. Here, we show that, in the presence of the allosteric inhibitor L-phenylalanine (Phe), the activator fructose 1,6-bisphosphate (FBP) can induce PKM2 tetramerisation, but fails to maximally increase enzymatic activity. Guided by a new computational framework we developed to identify residues that mediate FBP-induced allostery, we generated two PKM2 mutants, A327S and C358A, in which activation by FBP remains intact but cannot be attenuated by Phe. Our findings demonstrate a role for residues involved in FBP-induced allostery in enabling the integration of allosteric input from Phe and reveal a mechanism that underlies the co-ordinate regulation of PKM2 activity by multiple allosteric ligands.

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