Higher-level systematics of rodents and divergence time estimates based on two congruent nuclear genes

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Laonastes aenigmamus is an enigmatic rodent first described in 2005. Molecular and morphological data suggested that it is the sole representative of a new mammalian family, the Laonastidae, and a member of the Hystricognathi. However, the validity of this family is controversial because fossil-based phylogenetic analyses suggest that Laonastes is a surviving member of the Diatomyidae, a family considered to have been extinct for 11 million years. According to these data, Laonastes and Diatomyidae are the sister clade of extant Ctenodactylidae (i.e., gundies) and do not belong to the Hystricognathi. To solve the phylogenetic position of Laonastes, we conducted a large-scale molecular phylogeny of rodents. The analysis includes representatives of all major rodent taxonomic groups and was based on 5.5 kb of sequence data from four nuclear and two mitochondrial genes. To further validate the obtained results, a short interspersed element insertion analysis including 11 informative loci was also performed. Our molecular data based on sequence and short interspersed element analyses unambiguously placed Laonastes as a sister clade of gundies. All alternative hypotheses were significantly rejected based on ShimodairaHasegawa tests, supporting the idea that Laonastes does not belong to the Hystricognathi. Molecular dating analysis also supports an ancient divergence, Ϸ44 Mya ago, between Ctenodactylidae and Laonastes. These combined analyses support the hypothesis that Laonastes is indeed a living fossil. Protection of this surviving species would conserve an ancient mammalian family.Laonastes aenigmamus ͉ molecular phylogeny ͉ rodent ͉ retroposons

Section: Resultssupporting

confidence: 82%

Multiple molecular evidences for a living mammalian fossil

Huchon

Chevret

Jordan

et al. 2007

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163

“…Mouse ORF1p contains potential phosphorylation sites that correspond to positions S18, S27, S119, T203, T250, S254, and S287 in human ORF1p ( Fig. 1 and Table 1), suggesting that these sites have been conserved for at least 120 million years, the estimated time at which rodents and primates diverged (52).…”

Section: Resultsmentioning

confidence: 99%

Phosphorylation of ORF1p is required for L1 retrotransposition

Cook

Jones

Furano

2015

Although members of the L1 (LINE-1) clade of non-LTR retrotransposons can be deleterious, the L1 clade has remained active in most mammals for ∼100 million years and generated almost 40% of the human genome. The details of L1-host interaction are largely unknown, however. Here we report that L1 activity requires phosphorylation of the protein encoded by the L1 ORF1 (ORF1p). Critical phospho-acceptor residues (two serines and two threonines) reside in four conserved proline-directed protein kinase (PDPK) target sites. The PDPK family includes mitogen-activated protein kinases and cyclin-dependent kinases. Mutation of any PDPK phospho-acceptor inhibits L1 retrotransposition. The phosphomimetic aspartic acid can restore activity at the two serine sites, but not at either threonine site, where it is strongly inhibitory. ORF1p also contains conserved PDPK docking sites, which promote specific interaction of PDPKs with their targets. As expected, mutations in these sites also inhibit L1 activity. PDPK mutations in ORF1p that inactivate L1 have no significant effect on the ability of ORF1p to anneal RNA in vitro, an important biochemical property of the protein. We show that phosphorylated PDPK sites in ORF1p are required for an interaction with the peptidyl prolyl isomerase 1 (Pin1), a critical component of PDPK-mediated regulation. Pin1 acts via isomerization of proline side chains at phosphorylated PDPK motifs, thereby affecting substrate conformation and activity. Our demonstration that L1 activity is dependent on and integrated with cellular phosphorylation regulatory cascades significantly increases our understanding of interactions between L1 and its host.L 1 (or LINE-1) activity over the last ∼100 million years of primate evolution has generated ∼40% of the human genome (1, 2); thus, succeeding families of L1 elements are the main drivers of genetic expansion. These autonomously replicating elements convert their RNA transcripts and those of other genetic elements, particularly SINEs, into genomic DNA (3). A generic L1 element is 6-7 kb and contains the following: a 5′ UTR; ORF1, which encodes the coiled-coil mediated trimeric nucleic acid chaperone protein ORF1p; ORF2, which encodes a DNA endonuclease and reverse-transcriptase ORF2p; and a 3′ UTR terminated in a polyA sequence (reviewed in refs. 3 and 4). ORF1p, ORF2p, and L1 RNA form ribonucleoprotein particles (RNPs) that are likely intermediates in L1 retrotransposition (5-8). The L1-encoded proteins ORF1p and ORF2p are essential in cell culture-based retrotransposition assays (9) and in vitro assays using RNPs from cells transfected with L1 retrotransposition vectors (7). Although the role of ORF1p in retrotransposition is not known, mutations that affect its nucleic acid binding and chaperone activities can inactivate L1 (7, 9, 10).L1 activity can damage DNA (11), can generate genetic diversity and rearrangements (12-16), and is activated in certain tumors (17-19) and other somatic cells (20), including neuronal cells (21-23). Despite being deleterious (2...

“…Some have argued that phiomorphs and caviomorphs are likely to have shared a common Afro-Arabian ancestor (15)(16)(17), while others have suggested that the phiomorph-caviomorph split might have occurred in Asia, and that caviomorphs dispersed to South America either through Afro-Arabia or via a southern Gondwanan route (13,18). One critical issue that has hindered understanding of the group's historical biogeography is the phylogenetic position of the family Hystricidae, which has been placed as either the sister group of a phiomorph-caviomorph clade or as the sister group of Caviomorpha, in recent molecular phylogenetic analyses (9,(19)(20)(21). Temporal and tectonic constraints on competing biogeographic hypotheses have also been limited by radically different molecular estimates of the phiomorph-caviomorph split, which range in age from Ϸ85 Ma to Ϸ36 Ma (9,18,19,22,23).…”

mentioning

confidence: 99%

Fossil and molecular evidence constrain scenarios for the early evolutionary and biogeographic history of hystricognathous rodents

Sallam

Seiffert

Steiper

et al. 2009

The early evolutionary and paleobiogeographic history of the diverse rodent clade Hystricognathi, which contains Hystricidae (Old World porcupines), Caviomorpha (the endemic South American rodents), and African Phiomorpha (cane rats, dassie rats, and blesmols) is of great interest to students of mammalian evolution, but remains poorly understood because of a poor early fossil record. Here we describe the oldest well-dated hystricognathous rodents from an earliest late Eocene (Ϸ37 Ma) fossil locality in the Fayum Depression of northern Egypt. These taxa exhibit a combination of primitive and derived features, the former shared with Asian ''baluchimyine'' rodents, and the latter shared with Oligocene phiomorphs and caviomorphs. Phylogenetic analysis incorporating morphological, temporal, geographic, and molecular information places the new taxa as successive sister groups of crown Hystricognathi, and supports an Asian origin for stem Hystricognathi and an Afro-Arabian origin for crown Hystricognathi, stem Hystricidae, and stem Caviomorpha. Molecular dating of early divergences within Hystricognathi, using a Bayesian ''relaxed clock'' approach and multiple fossil calibrations, suggests that the split between Hystricidae and the phiomorphcaviomorph clade occurred Ϸ39 Ma, and that phiomorphs and caviomorphs diverged Ϸ36 Ma. These results are remarkably congruent with our phylogenetic results and the fossil record of hystricognathous rodent evolution in Afro-Arabia and South America.