A RhoGAP protein as a main immune suppressive factor in the Leptopilina boulardi (Hymenoptera, Figitidae)–Drosophila melanogaster interaction

2005 ◽  
Vol 35 (2) ◽  
pp. 93-103 ◽  
Author(s):  
C. Labrosse ◽  
K. Stasiak ◽  
J. Lesobre ◽  
A. Grangeia ◽  
E. Huguet ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Leptopilina Boulardi

scholarly journals Mapping candidate genes for Drosophila melanogaster resistance to the parasitoid wasp Leptopilina boulardi

2006 ◽  
Vol 88 (2) ◽  
pp. 81-91 ◽  
Author(s):  
M. HITA ◽  
E. ESPAGNE ◽  
F. LEMEUNIER ◽  
L. PASCUAL ◽  
Y. CARTON ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Candidate Genes ◽  
Resistance Gene ◽  
Molecular Level ◽  
Single Gene ◽  
Parasitoid Wasp ◽  
Male Recombination ◽  
Leptopilina Boulardi

Drosophila melanogaster resistance against the parasitoid wasp Leptopilina boulardi is under the control of a single gene (Rlb), with two alleles, the resistant one being dominant. Using strains bearing deletions, we previously demonstrated that the 55E2–E6; 55F3 region on chromosome 2R is involved in the resistance phenomenon. In this paper, we first restricted the Rlb containing region by mapping at the molecular level the breakpoints of the Df(2R)Pc66, Df(2R)P34 and Df(2R)Pc4 deficiencies, using both chromosomal in situ hybridization and Southern analyses. The resistance gene was localized in a 100 kb fragment, predicted to contain about 10 different genes. Male recombination genetic experiments were then performed, leading to identification of two possible candidates for the Rlb gene. Potential involvement of one of this genes, edl/mae, is discussed.

scholarly journals Genetic Localization of a Drosophila melanogaster Resistance Gene to a Parasitoid Wasp and Physical Mapping of the Region

1999 ◽  
Vol 9 (5) ◽  
pp. 471-481
Author(s):  
Maria Teresa Hita ◽  
Maryléne Poirié ◽  
Nathalie Leblanc ◽  
Francoise Lemeunier ◽  
Francoise Lutcher ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Physical Mapping ◽  
Physical Map ◽  
Single Gene ◽  
Parasitoid Wasp ◽  
Restriction Map ◽  
Cross Hybridization ◽  
Restriction Fragments ◽  
Leptopilina Boulardi ◽  
The Right

Drosophila melanogaster larvae usually react against eggs of the parasitoid wasp Leptopilina boulardi by surrounding them with a multicellular melanotic capsule. The genetic determinism of this response has been studied previously using susceptible (non-capsule-forming) and resistant (capsule-forming) strains. The results suggest that differences in their encapsulation response involve a single gene, resistance to Leptopilina boulardi(Rlb), with two alleles, the resistant one being dominant.Rlb confers specific protection against Leptopilina boulardi and is thus probably involved in parasitoid recognition. Recent studies have localized this gene on the right arm of the second chromosome and our aim was to precisely determine its genetic and molecular location. Using strains bearing deletions, we demonstrated that resistance to Leptopilina boulardi is conferred by the55C; 55F3 region and that the 55E2–E6; F3 region is particularly involved. A physical map of the 55C;56A region was then constructed, based on a set of overlapping cosmid and P1 phage clones. Using single and double digests, cross hybridization of restriction fragments, and location of genetically mapped genes and STSs, a complete, five-enzyme restriction map of this 830-kb region was obtained.

Insect immunity: early events in the encapsulation process of parasitoid (Leptopilina boulardi) eggs in resistant and susceptible strains of Drosophila

Parasitology ◽  
1996 ◽  
Vol 112 (1) ◽  
pp. 135-142 ◽  
Author(s):  
J. Russo ◽  
S. Dupas ◽  
F. Frey ◽  
Y. Carton ◽  
M. Brehelin
Keyword(s):  
Drosophila Melanogaster ◽  
Resistant Strain ◽  
Egg Laying ◽  
Insect Immunity ◽  
Dense Layer ◽  
Cell Necrosis ◽  
Leptopilina Boulardi ◽  
Initial Event ◽  
Encapsulation Process ◽  
Drosophila Yakuba

SUMMARYEggs of an immune suppressive strain ( = virulent) of the parasitoid Leptopilina boulardi are encapsulated neither in resistant nor in susceptible strains of Drosophila melanogaster but are encapsulated in Drosophila yakuba. Eggs of a non-immune suppressive strain ( = avirulent) of the same parasitoid are encapsulated in a resistant strain of D. melanogaster and in D. yakuba but are not encapsulated in a susceptible strain of D. melanogaster. Egg chorion in the 2 parasitoid strains showed the same morphology and the same modifications after egg laying whatever the host strain. When a capsule is built, a small dotted dense layer was first spread on the chorion, followed by accumulation layers of cells (plasmatocytes and lamellocytes) and lastly necrosis of the inner haemocytes. The encapsulated eggs darken only at the time of necrosis of haemocytes. In susceptible hosts, neither the tiny dense layer nor haemocyte accumulation occured. We concluded that (1) this tiny dense layer was present before the deposition of the first haemocytes, (2) inhibition of deposition of this dense layer was the initial event of the induced immunosupression, (3) haemocytes other than lamellocytes were engaged in caspsule formation, (4) the immunosupressive factors did not target only the lamellocytes but also the plasmatocytes, (5) darkening of the encapsulated eggs was due to cell necrosis rather than to extracellular melanin deposition.

scholarly journals Symbiont-mediated fly survival is independent of defensive symbiont genotype in the Drosophila melanogaster-Spiroplasma-wasp interaction

2020 ◽  
Author(s):  
Jordan E. Jones ◽  
Gregory D. D. Hurst
Keyword(s):  
Drosophila Melanogaster ◽  
Laboratory Experiment ◽  
Common Garden ◽  
Insect Host ◽  
Protective Capacity ◽  
Protective Efficiency ◽  
Leptopilina Heterotoma ◽  
Leptopilina Boulardi ◽  
Contrast Analysis ◽  
Per Se

AbstractWhen a parasite attacks an insect, the outcome is commonly modulated by the presence of defensive heritable symbionts residing within the insect host. Previous studies noted markedly different strengths of Spiroplasma-mediated fly survival following attack by the same strain of wasp. One difference between the two studies was the strain of Spiroplasma used. We therefore performed a common garden laboratory experiment to assess whether Spiroplasma-mediated protection depends upon the strain of Spiroplasma. We perform this analysis using the two strains of male-killing Spiroplasma used previously, and examined response to challenge by two strains of Leptopilina boulardi and two strains of Leptopilina heterotoma wasp. We found no evidence Spiroplasma strain affected fly survival following wasp attack. In contrast, analysis of the overall level of protection, including the fecundity of survivors of wasp attack, did indicate the two Spiroplasma strains tested varied in protective efficiency against three of the four wasp strains tested. These data highlight the sensitivity of symbiont-mediated protection phenotypes to laboratory conditions, and the importance of common garden comparison. Our results also indicate that Spiroplasma strains can vary in protective capacity in Drosophila, but these differences may exist in the relative performance of survivors of wasp attack, rather than in survival of attack per se.

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