Tuesday, February 28, 2006
Wolbachia 101
For the past year, I've been studying associations between insects and Wolbachia, symbiotic bacteria which live inside the cells of arthropods and nematodes. The topic is huge in both depth and breadth, but I'll attempt a brief and simple overview.
Wolbachia are vertically transmitted, which means they pass from parent to offspring. Specifically, they are normally found within the cells of insect reproductive organs, and pass from mother to offspring through the cytoplasm of egg cells; sperm cells, which have little cytoplasm, rarely if ever transmit the bacteria. The association between Wolbachia and insect cells is an obligate one; these are not bacteria that you can streak out on an agar plate.
This tight association means that it's to Wolbachia's evolutionary advantage to manipulate the reproduction of the host, so as to make more daughters that will pass Wolbachia along through the next generation. There are four main ways in which Wolbachia does this.
One way is through the Wolbachia F phenotype, which stands for feminization of genetic males. This phenotype is known in isopod crustaceans (common "pillbugs" and "sowbugs", which are not insects). These arthropods normally have what is called a "ZW" sex determination system. ZW is kind of like our XY system, only backwards; females are "heterogametic", having one Z and one W chromosome, while males are "homogametic" and have two Zs. Wolbachia-infected individuals develop as females, even if they have what would normally be the male ZZ genotype.
Another phenotype is parthenogenesis induction, or PI. This phenotype is best known in parasitoid wasps, tiny insects that lay eggs in the bodies of other arthropods. In infected mothers, the genetic material of the gamete (egg) is duplicated instead of requiring fertilization, and these eggs give rise to diploid daughters. In some of these species, males were unknown until researchers "cured' the Wolbachia infection by giving antibiotics to females. The females then produced unfertilized eggs that developed into haploid males.
A third phenotype, male-killing (MK) does exactly what it sounds like; infected male embryos die early in development. This situation becomes complicated, because it doesn't imply parthenogenesis. Infected mothers put all of their resources into daughter production, and if males can mate more than once, making lots of daughters ensures lots of grandchildren (and more Wolbachia). However, if MK infections become highly prevalent, mates for all these females become scarce, which is favorable to uninfected mothers because sons now become more valuable. For obvious reasons, MK infections don't usually sweep through a population. Under some circumstances, the infection can reach an equilibrium frequency in an arthropod population.
The fourth phenotype is cytoplasmic incompatibility, or CI. The briefest way to describe CI: An infected female can mate successfully with any male, but an uninfected female can reproduce successfully only with an uninfected male. In CI infections, Wolbachia in a male apparently modifies sperm so that it requires "rescue" by the bacteria in an infected egg. Match this altered sperm with an uninfected egg, and the fertilization fails. The result: Infected females have broader mating opportunities than uninfected females, and tend to leave more offspring. Again, a win for Wolbachia, which hitchhike along with the infected daughters.
The molecular and cellular mechanisms by which Wolbachia does its stuff are active research topics. So are its ecological dynamics and consequences, since it can shift sex ratios in an insect population, contribute to the split of one population into two reproductive isolates, or even change phenotype (for example, from CI to MK) in the process of infecting new host species (which it sometimes does, even though it's usually only vertically transmitted). There is considerable genetic diversity among Wolbachia strains, though, and in some cases multiple bacterial strains are found in the same insect species, or even in the same individual.
So, although I'm not a microbiologist (nor do I play one on TV), I spend a lot of time in the lab testing insects for an infection that requires a better microscopist than myself to actually see. Fortunately, we fanciers of multi-cellular eukaryotes can use the polymerase chain reaction (PCR) to amplify Wolbachia genes from preparations of ground-up, infected insects. By current estimates, around 20% of all insect species may be infected, although some estimates are considerably higher, especially since some species may have rare infections that don't show up in the samples collected for PCR screening.
Wolbachia will undoubtedly pop up again in these pages. And, so will the sex determination systems of wasps, ants, and bees. ("Wait a minute ... haploid males? How did they do that? ")
Watch this space!
Wolbachia are vertically transmitted, which means they pass from parent to offspring. Specifically, they are normally found within the cells of insect reproductive organs, and pass from mother to offspring through the cytoplasm of egg cells; sperm cells, which have little cytoplasm, rarely if ever transmit the bacteria. The association between Wolbachia and insect cells is an obligate one; these are not bacteria that you can streak out on an agar plate.
This tight association means that it's to Wolbachia's evolutionary advantage to manipulate the reproduction of the host, so as to make more daughters that will pass Wolbachia along through the next generation. There are four main ways in which Wolbachia does this.
One way is through the Wolbachia F phenotype, which stands for feminization of genetic males. This phenotype is known in isopod crustaceans (common "pillbugs" and "sowbugs", which are not insects). These arthropods normally have what is called a "ZW" sex determination system. ZW is kind of like our XY system, only backwards; females are "heterogametic", having one Z and one W chromosome, while males are "homogametic" and have two Zs. Wolbachia-infected individuals develop as females, even if they have what would normally be the male ZZ genotype.
Another phenotype is parthenogenesis induction, or PI. This phenotype is best known in parasitoid wasps, tiny insects that lay eggs in the bodies of other arthropods. In infected mothers, the genetic material of the gamete (egg) is duplicated instead of requiring fertilization, and these eggs give rise to diploid daughters. In some of these species, males were unknown until researchers "cured' the Wolbachia infection by giving antibiotics to females. The females then produced unfertilized eggs that developed into haploid males.
A third phenotype, male-killing (MK) does exactly what it sounds like; infected male embryos die early in development. This situation becomes complicated, because it doesn't imply parthenogenesis. Infected mothers put all of their resources into daughter production, and if males can mate more than once, making lots of daughters ensures lots of grandchildren (and more Wolbachia). However, if MK infections become highly prevalent, mates for all these females become scarce, which is favorable to uninfected mothers because sons now become more valuable. For obvious reasons, MK infections don't usually sweep through a population. Under some circumstances, the infection can reach an equilibrium frequency in an arthropod population.
The fourth phenotype is cytoplasmic incompatibility, or CI. The briefest way to describe CI: An infected female can mate successfully with any male, but an uninfected female can reproduce successfully only with an uninfected male. In CI infections, Wolbachia in a male apparently modifies sperm so that it requires "rescue" by the bacteria in an infected egg. Match this altered sperm with an uninfected egg, and the fertilization fails. The result: Infected females have broader mating opportunities than uninfected females, and tend to leave more offspring. Again, a win for Wolbachia, which hitchhike along with the infected daughters.
The molecular and cellular mechanisms by which Wolbachia does its stuff are active research topics. So are its ecological dynamics and consequences, since it can shift sex ratios in an insect population, contribute to the split of one population into two reproductive isolates, or even change phenotype (for example, from CI to MK) in the process of infecting new host species (which it sometimes does, even though it's usually only vertically transmitted). There is considerable genetic diversity among Wolbachia strains, though, and in some cases multiple bacterial strains are found in the same insect species, or even in the same individual.
So, although I'm not a microbiologist (nor do I play one on TV), I spend a lot of time in the lab testing insects for an infection that requires a better microscopist than myself to actually see. Fortunately, we fanciers of multi-cellular eukaryotes can use the polymerase chain reaction (PCR) to amplify Wolbachia genes from preparations of ground-up, infected insects. By current estimates, around 20% of all insect species may be infected, although some estimates are considerably higher, especially since some species may have rare infections that don't show up in the samples collected for PCR screening.
Wolbachia will undoubtedly pop up again in these pages. And, so will the sex determination systems of wasps, ants, and bees. ("Wait a minute ... haploid males? How did they do that? ")
Watch this space!
