Reports

HOPE Report No.1 2004-07-07

Program No.1 (Joint research)

Oral presentation on "The DNA Sequence of Chimpanzee Chromosome 22 and Comparative Analysis with Human Chromosome 21" in the workshop of "Primate Genomics" in HGM2004 in Berlin and the discussion with Dr. Svante Pääbo about the speciation of chimpanzees and bonobos.

By Hidemi Watanabe

Place of visit: Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany.

Period of visit: 15th-21th MApril 2004

I attended the HGM2004in Berlin. In April 5th, 2004. I participated in the workshop titled "Primate Genomics" and gave a talk on "The DNA Sequence of Chimpanzee Chromosome 22 and Comparative Analysis with Human Chromosome 21". 

This is an outcome of the collaborative research with Dr. Svante Pääbo and his colleagues in MPIEVA. After the congress, I talked with Dr. Pääbo on the speciation of chimpanzees and bonobos in relation to the potential influence of the geographical separation by the formation of Congo River. 

The summary of my talk was as follows. To backtrack the genomic changes during human evolution, we have decided to sequence chimpanzee genomes and recently sequenced chimpanzee chromosome 22 (PTR22), the orthologous chromosome of human chromosome 21 (HSA21). Through the comparison between HSA21 and PTR22, we revealed a large number of differences between them. Surprisingly enough, 50% of the genes in these chromosomes showed differences in their amino acid sequences, though the nucleotide difference level was around 1%.

 We further sequenced the genomic portions in gorillas and orangutans that corresponded to some of the differences, and we inferred the states of these loci in the LCA of humans and chimpanzees with a cladistical way and revealed the evolutionary events occurred in the human and the chimpanzee lineages. One of the significant differences between these lineages was the frequency of Alu and L1PA2 insertions. We found many differences in the expression and the structures of genes that were involved in immune systems, implying that these differences are the cause of the phenotypic differences in susceptibilities to various infectious diseases.

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