Abstract
Cytoplasmic incompatibility (CI) is the most common symbiont-induced reproductive manipulation. Specifically, symbiont-induced sperm modifications cause catastrophic mitotic defects in the fertilized embryo and ensuing lethality in crosses between symbiotic males and either aposymbiotic females or females harboring a different symbiont strain. However, if the female carries the same symbiont strain, then embryos develop properly, thereby imparting a relative fitness benefit to symbiont-transmitting mothers. Thus, CI drives maternally-transmitted bacteria to high frequencies in arthropods worldwide. In the past two decades, CI experienced a boom in interest due to its (i) deployment in worldwide efforts to curb mosquito-borne diseases, (ii) causation by bacteriophage genes, cifA and cifB, that modify sexual reproduction, and (iii) important impacts on arthropod speciation. This review serves as a gateway to experimental, conceptual, and quantitative themes of CI and outlines significant gaps in understanding CI’s mechanism that are ripe for investigation from diverse subdisciplines in the life sciences.
Highlights
From 1938 through the 1960s, an enigmatic, intraspecific incompatibility that caused embryonic death was reported between geographically isolated strains of Culex pipiens mosquitoes (Laven, 1951; Marshall, 1938), Aedes scutellaris mosquitoes (Smith-White and Woodhill, 1955), and Nasonia vitripennis parasitoid wasps (Ryan and Saul, 1968)
Motivated by the finding that Typhus is a Rickettsial disease (Rocha-Lima, 1916), microbiologists Hertig and Wolbach conducted a survey of Rickettsia-like bacteria among numerous arthropod orders in and around Boston, Massachusetts in 1924 (Hertig and Wolbach, 1924)
Wolbachia were first discovered in Cu. pipiens mosquitoes in 1924 and were later linked to cytoplasmic incompatibility (CI) in 1973 (Hertig and Wolbach, 1924; Yen and Barr, 1973)
Summary
From 1938 through the 1960s, an enigmatic, intraspecific incompatibility that caused embryonic death was reported between geographically isolated strains of Culex pipiens mosquitoes (Laven, 1951; Marshall, 1938), Aedes scutellaris mosquitoes (Smith-White and Woodhill, 1955), and Nasonia vitripennis parasitoid wasps (Ryan and Saul, 1968). Population genetic analyses of cif genes in wPip reveal that there are numerous unique strains, each strain carries multiple closely related cif variants that belong to Type 1 and Type 4 cif clades, and a single genetic variant of CifBwPip[T1] correlates with the inability of one strain of wPip to rescue CI caused by a divergent wPip strain (Atyame et al, 2011b; Bonneau et al, 2018a, 2019) While these data suggest that cif genetic variation and/or copy number contributes to strain incompatibility, it remains possible that the considerable host genotypic variation between these incompatible populations 370 contributes to these relationships in a way that correlates with cif genotypic diversity (Atyame et al, 2011a). Functional validation that divergent Cif proteins are functional, that they have differential impacts on the host, and contribute summatively to incompatibilities are lacking
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