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Intelligent Language of Genes

Majid Ali, M.D.

 

In 2001, the Human Genome Project Consortium estimated the number of genes in the human genome to be over 31,000, while Celera Genomics established that number to be 26,588, with 12,731 candidate genes.1-5 Implication of this work have been recently presented in special issues of Nature and Science.6-15 It is safe to predict that the knowledge of human genome—and, equally significantly, that of proteomics—will radically alter the way we think of the disease/dis-ease.disease.

A mouse genome has a few thousand less genes, and that of a fruit fly about one third of that. By the gene numbers game, a human equals a mouse plus one tenth of a fruit fly. Even a lowly roundworm (Caenorhabditis elegans) contains only one third less genes than we humans. This nematode contains a total number of 959 cells, of which 302 are neurons that make up its brain. By contrast, humans have an estimated 100 trillion cells in the body, of which 100 billion are neurons. That raises some interesting questions: With only one third additional genes, how did the human brain get so many more brain cells (100 billion less 302) than the roundworm? And, how with such a small number of additional genes, does the human genome control the generation, development, differentiation, and orderly death (apoptosis) of such an enormous number of brain cells?

We are also told that a human genome is like a chopped, churned, and rearranged mouse genome—not very flattering for the species that has long claimed to occupy the apex of the hierarchy of living beings. Evidently, neither the cellular DNA mass nor the number of genes accounts for the sophistication of human biology. If not in the number of genes and the mass of DNA, where do we look for an explanation? This is one of the areas in which nature is at its most eloquent in its mastery of molecular complementarity and contrariety.

Gene expression comprises initial transcription in the nucleus and subsequent translation of mRNA in the cytoplasm. The cargo of gene products (proteins) is shuttled within the intracellular compartments by highly complex and finely orchestrated mechanisms involving vesicles that form by budding from the donor organelle, are transported to an acceptor organelle, dock with specific sites of delivery, and finally fuse with the target organelle for unloading. The protein families that control vesicle traffic are highly conserved through phylogeny from yeast to fruit fly to mouse to man. Some measure of the genetic complexity of vesicular traffic can be gained by simply considering the number (in hundreds) and range of proteins (extremely broad) involved with such traffic.16

Single nucleotide polymorphisms (SNPs), as is implicit in the name, are locations in the genome where individuals vary by a single genetic letter.17 It has been estimated that there are over two million SNPs in the human genome. What are the biologic implications of such a vast number of SNPs? That question probably will be never answered in full, given the accelerating rate of changes in ecologic conditions that lead to alteration in the genome.

There are three human cytoskeletal systems involved in the development, structural integrity, motility, and other diverse aspects of cell membranes: actin filaments, microtubules, and intermediate filaments. More than 70 families of actin-binding proteins, over a dozen families of microtubule-binding proteins, and over 30 human intermediate filament proteins were identified at the time of the initial reports of the human genome in February 2001.18 No one can venture at this time how many members there might be in any of those families or how many other families remain to be discovered.

Another glimpse into genetic complementarity and contrariety may be obtained by considering the genetic underpinnings of cancer. All cancers are characterized by disruptions of the genome and caused by alterations in DNA sequence. The number of oncogenes that trigger carcinogenesis is steadily increasingly. Over 30 recessive oncogenes (tumor suppressor genes) and over one hundred dominant genes were identified by February 2001.19 Undoubtedly, there will be more.

There are, of course, several other issues. The number of human mRNA species—estimated from various assemblies of expressed sequence tags (EST)—is 85,000, greater than twice that of genes.20 That discrepancy remains unresolved and may turn out to be of considerable significance. The estimated number of human cDNA species is also much larger than the proposed gene number and thought to be up to 48,000. Computer models have predicted up to 46,000 unigene EST clusters for which there was no evidence of protein-coding potential.21,22 Attempts have been made to explain the excess of cDNA/EST clusters over recognized protein-coding genes by invoking the presence of a large number of alternative forms of protein-coding transcripts along with numerous transcripts from uncharacterized, non-protein-coding "genes," such as Xist and H19. Such genes are discovered by chance rather than by the approaches designated ab initio gene-finding programs.

At this time, the coding regions of genes, called exons, appear to account for only 3% of DNA.23 Exons are split into pieces in the genome and these pieces are separated by non-coding sequences called introns. Repeat sequences, with or without a function, form approximately 46% of the genome. The remainder of the genome contains promotes, transcriptional regulatory sequences, and almost certainly other features that remain to be discovered.

The structure, function, and evolution of genes have been examined by the following: (1) morphology of chromosomes (both normal and abnormal); (2) construction of genomic landmarks; (3) observation of genetic transmission of phenotypes; (4) study of DNA sequence variations; and (5) characterization of individual genes. Genes have been discovered by finding putative orthologues (related to a gene in another species) and paralogues (family members derived by gene duplications).

Repetitive sequences with an excess of cytosines and guanines show a tendency to clustering in the vicinity of genes while those rich in nucleotides adenine and thymine are found in abundance in the gene-poor regions ("deserts") in chromosomes. That explains the distinctive light and dark banding patterns of chromosomes. The dark bands are generally gene-poor zones dominated by adenines and thymines, while the light bands are usually composed of gene-rich regions with a higher concentration of cytosines and guanines. The uneven gene distribution also accounts for some small chromosomes (for example, chromosome 19) having a disproportionately large number of genes. Indeed, such "ruggedness of terrain" distinguishes the human genome from genomes of some other species that show lesser degrees of gene clustering.

Pseudogenes

There is also the matter of pseudogenes, sequences that at first sight look like genes but lack paraphernalia to persuade the cells that host them to transcribe them. At present pseudogenes are so designated because matching proteins (encoded by them) are thought not to exist. This is one reason why estimates of the total number of genes in the human genome vary so much. Future work is likely to lead to recognition of many matching proteins and redesignation of sequences now considered pseudogenes as true genes.

Related Articles

* Genetics

* Re-Thinking DNA

* Intelligent language of Genes

* Junk DNA or Treasure trove

* Genes Know Their Neighbors

* A Story of Interleukins and Tumor Necrosis Genes

* Genes and Aging

* Of Genes, Chimps, and Men

 

* Genes and Aging

 

 

 

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