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From chloroplasts to “cryptic” plastids: evolution of plastid genomes in parasitic plants

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Abstract

To date, more than 130 plastid genomes (plastomes) have been completely sequenced. Of those, 12 are strongly reduced plastid genomes from heterotrophic plants or plant-related species that exhibit a parasitic lifestyle. Half of these species are land plants while the other half consists of unicellular species that have evolved from photosynthetic algae. Due to their specialized lifestyle, parasitic lineages experienced a loss of evolutionary pressure on the plastid genome and, in particular, on the photosynthesis-related genes. This made them tolerant for the accumulation of detrimental mutations and deletions in plastid genes. That parasitic plants are naturally occurring plastome mutants makes them a rich source of information concerning plastome evolution and the mechanisms that are involved. This review reports on the progress made in recent years with parasitic plant plastomes and attempts to summarize what we can learn from analysing the genomes of functionally reduced, or cryptic, plastids. Particularly, the loss of genes for a plastid-encoded RNA polymerase as well as an intron maturase and the retention of the gene for the large subunit of the Calvin cycle enzyme Ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) in selected species will be discussed.

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Abbreviations

bp:

Basepairs

NEP:

Nuclear-endoded RNA polymerase

PEP:

Plastid encoded RNA polymerase

Rubisco:

Ribulose-1,5-bisphosphate carboxylase/oxygenase

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Acknowledgments

The suggestions made by T.V. Bhuvaneswari (University of Tromsø) regarding the text and the concept of the manuscript are highly appreciated. In addition, K. Fischer (University of Tromsø) and K. Krupinska (University of Kiel) are thanked for their constructive comments during preparation of the manuscript.

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Correspondence to Kirsten Krause.

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Communicated by R. Bock.

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Krause, K. From chloroplasts to “cryptic” plastids: evolution of plastid genomes in parasitic plants. Curr Genet 54, 111–121 (2008). https://doi.org/10.1007/s00294-008-0208-8

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