We have collected a set of 347 proteins that are found in eukaryotic cells but have no significant homology to proteins in Archaea and Bacteria. We call these proteins eukaryotic signature proteins (ESPs). The dominant hypothesis for the formation of the eukaryotic cell is that it is a fusion of an archaeon with a bacterium. If this hypothesis is accepted then the three cellular domains, Eukarya, Archaea, and Bacteria, would collapse into two cellular domains. We have used the existence of this set of ESPs to test this hypothesis. The evidence of the ESPs implicates a third cell (chronocyte) in the formation of the eukaryotic cell. The chronocyte had a cytoskeleton that enabled it to engulf prokaryotic cells and a complex internal membrane system where lipids and proteins were synthesized. It also had a complex internal signaling system involving calcium ions, calmodulin, inositol phosphates, ubiquitin, cyclin, and GTP-binding proteins. The nucleus was formed when a number of archaea and bacteria were engulfed by a chronocyte. This formation of the nucleus would restore the three cellular domains as the Chronocyte was not a cell that belonged to the Archaea or to the Bacteria.
We compared intron-exon structures in 1,560 human-mouse orthologs and 360 mouse-rat orthologs. The origin of differences in intron positions between species was inferred by comparison with an outgroup, Fugu for human-mouse and human for mouse-rat. Among 10,020 intron positions in the human-mouse comparison, we found unequivocal evidence for five independent intron losses in the mouse lineage but no evidence for intron loss in humans or for intron gain in either lineage. Among 1,459 positions in ratmouse comparisons, we found evidence for one loss in rat but neither loss in mouse nor gain in either lineage. In each case, the intron losses were exact, without change in the surrounding coding sequence, and involved introns that are extremely short, with an average of 200 bp, an order of magnitude shorter than the mammalian average. These results favor a model whereby introns are lost through gene conversion with intronless copies of the gene. In addition, the finding of widespread conservation of intron-exon structure, even over large evolutionary distances, suggests that comparative methods employing information about gene structures should be very successful in correctly predicting exon boundaries in genomic sequences. When it was discovered 25 years ago that eukaryotes, unlike prokaryotes, had split gene structures, it came as quite a shock. Where did these so-called introns come from? What uses did they have? How did they propagate? How labile were their positions and sequences? These are questions that have proved very difficult to solve despite occupying the minds and laboratories of a generation of biologists.As the exon-intron structure of genes reaches its silver anniversary, much about this structure is still a mystery and the subject of intense research. In this postgenomic world, introns have proven themselves a singular pest in our attempts to predict gene structures from raw genome sequence. They have almost no consensus sequence over their lengths; they can be absurdly long; and they are the substrates of a bewildering array of different alternative splicing patterns. One promising avenue of improvement of the algorithms would further exploit comparisons with other genomic sequences. If intron-exon structures are highly conserved between two species, the viability of an exon prediction should be able to be evaluated by comparison with the orthologous gene copy in another organism.However, before such comparisons can be used, it is important to know more about the degree of conservation of gene structure between related species. Two ill understood processes that may change the intron-exon structure of genes are intron loss, in which the intervening noncoding sequence between two exons is jettisoned, and intron gain, in which an intron appears de novo. Apparent instances of both have been described. The first such event was characterized by Perler et al.(1) in 1980. Rats have two insulin genes, one with a two-exon-one-intron structure and the other with a three-exon-two-intron structure (in which one i...
We purge large databases of animal, plant, and fungal introncontaining genes to a 20% similarity level and then identify the most similar animal-plant, animal-fungal, and plant-fungal protein pairs. We identify the introns in each BLAST 2.0 alignment and score matched intron positions and slid (near-matched, within six nucleotides) intron positions automatically. Overall we find that 10% of the animal introns match plant positions, and a further 7% are ''slides.'' Fifteen percent of fungal introns match animal positions, and 13% match plant positions. Furthermore, the number of alignments with high numbers of matches deviates greatly from the Poisson expectation. The 30 animal-plant alignments with the highest matches (for which 44% of animal introns match plant positions) when aligned with fungal genes are also highly enriched for triple matches: 39% of the fungal introns match both animal and plant positions. This is strong evidence for ancestral introns predating the animal-plant-fungal divergence, and in complete opposition to any expectations based on random insertion. In examining the slid introns, we show that at least half are caused by imperfections in the alignments, and are most likely to be actual matches at common positions. Thus, our final estimates are that Ϸ14% of animal introns match plant positions, and that Ϸ17-18% of fungal introns match animal or plant positions, all of these being likely to be ancestral in the eukaryotes.exon ͉ phase distribution ͉ evolution ͉ eukaryote ͉ prokaryote I ntrons are prevalent in the complex eukaryotes but rare in the simple ones. Are these introns ancestral in all of the eukaryotes or do they arise as the organisms become more complex? Introns can be acquired by or eliminated from a gene during evolution, but what is the balance?An introns-late view argues that introns arise as ''selfish'' elements that play no constructive role in evolution. On this picture, introns appear relatively late in the evolution of eukaryotes (1-3) and spread as mobile elements that invade genes by insertion into short Ϸ4-to 5-nt-long ''proto-splice sites'' (4) (although the notion of proto-splice sites has been challenged; refs. 5 and 6).An introns-early theory suggests that introns made an essential contribution to the evolution of genes via ''exon shuffling,'' which created genes from exon ''pieces'' by recombination within the introns (7-12). In this view, introns existed before any eukaryote-prokaryote divergence, and since that time, the prokaryotic lineage completely lost its introns, whereas they were retained in the eukaryotes.The sequences within the introns change during evolution, far more rapidly than those of the exons. The only conserved elements are the short sequences at the 5Ј and 3Ј termini, which are very similar for all introns. The rest of the intron sequence appears neutral to selection, and the length of the intron sequence can change by orders of magnitude. However, the position of an intron in a gene's coding sequence is well conserved. If one compares the e...
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