Number Of Human Genes Research Articles

Mapping of PARK2 and PACRG Overlapping Regulatory Region Reveals LD Structure and Functional Variants in Association with Leprosy in Unrelated Indian Population Groups

Leprosy is a chronic infectious disease caused by Mycobacterium Leprae, where the host genetic background plays an important role toward the disease pathogenesis. Various studies have identified a number of human genes in association with leprosy or its clinical forms. However, non-replication of results has hinted at the heterogeneity among associations between different population groups, which could be due to differently evolved LD structures and differential frequencies of SNPs within the studied regions of the genome. A need for systematic and saturated mapping of the associated regions with the disease is warranted to unravel the observed heterogeneity in different populations. Mapping of the PARK2 and PACRG gene regulatory region with 96 SNPs, with a resolution of 1 SNP per 1 Kb for PARK2 gene regulatory region in a North Indian population, showed an involvement of 11 SNPs in determining the susceptibility towards leprosy. The association was replicated in a geographically distinct and unrelated population from Orissa in eastern India. In vitro reporter assays revealed that the two significantly associated SNPs, located 63.8 kb upstream of PARK2 gene and represented in a single BIN of 8 SNPs, influenced the gene expression. A comparison of BINs between Indian and Vietnamese populations revealed differences in the BIN structures, explaining the heterogeneity and also the reason for non-replication of the associated genomic region in different populations.

STAU1 binding 3' UTR IRAlus complements nuclear retention to protect cells from PKR-mediated translational shutdown.

For a number of human genes that encode transcripts containing inverted repeat Alu elements (IRAlus) within their 3' untranslated region (UTR), product mRNA is efficiently exported to the cytoplasm when the IRAlus, which mediate nuclear retention, are removed by alternative polyadenylation. Here we report a new mechanism that promotes gene expression by targeting mRNAs that maintain their 3' UTR IRAlus: Binding of the dsRNA-binding protein Staufen1 (STAU1) to 3' UTR IRAlus inhibits nuclear retention so as to augment the nuclear export of 3' UTR IRAlus-containing mRNAs (IRAlus mRNAs). Moreover, we found that 3' UTR IRAlus-bound STAU1 enhances 3' UTR IRAlus mRNA translation by precluding protein kinase R (PKR) binding, which obviates PKR activation, eukaryotic translation initiation factor 2α (eIF2α) phosphorylation, and repression of global cell translation. Thus, STAU1 binding to 3' UTR IRAlus functions along with 3' UTR IRAlus-mediated nuclear retention to suppress the shutdown of cellular translation triggered by PKR binding to endogenous cytoplasmic dsRNAs. We also show that a changing STAU1/PKR ratio contributes to myogenesis via effects on the 3' UTR IRAlus of mRNA encoding the microRNA-binding protein LIN28.

Are all of the human exons alternatively spliced?

Alternative mRNA splicing (AS) is a major mechanism for increasing regulatory complexity. A key concept in AS is the distinction between alternatively and constitutively spliced exons (ASEs and CSEs, respectively). ASEs and CSEs have been reported to be differentially regulated, and to have distinct biological properties. However, the recent flood of RNA-sequencing data has obscured the boundary between ASEs and CSEs. Researchers are beginning to question whether ‘authentic CSEs’ do exist, and whether the ASE/CSE distinction is biologically invalid. Here, I examine the influences of increasing transcriptome data on the human ASE/CSE classification and our past understanding of the properties of these two types of exons. Interestingly, although the percentage of human ASEs has increased dramatically in recent years, the overall distinction between ASEs and CSEs remain valid. For example, CSEs are longer, evolve more slowly, and less frequently correspond to intrinsically disordered protein regions than ASEs. In addition, only a relatively small number of human genes have their transcripts composed entirely of ASEs despite the large amount of high-throughput transcriptome information. Therefore, the ‘backbone’ concept of AS, in which CSEs constitute the invariant part and ASEs the flexible part of the transcript, appears to be generally true despite the increasing percentage of ASEs in the human exome.

Neuromuscular Disorders in Zebrafish: State of the Art and Future Perspectives

Neuromuscular disorders are a broad group of inherited conditions affecting the structure and function of the motor system with polymorphic clinical presentation and disease severity. Although individually rare, collectively neuromuscular diseases have an incidence of 1 in 3,000 and represent a significant cause of disability of the motor system. The past decade has witnessed the identification of a large number of human genes causing muscular disorders, yet the underlying pathogenetic mechanisms remain largely unclear, limiting the developing of targeted therapeutic strategies. To overcome this barrier, model systems that replicate the different steps of human disorders are increasingly being developed. Among these, the zebrafish (Danio rerio) has emerged as an excellent organism for studying genetic disorders of the central and peripheral motor systems. In this review, we will encounter most of the available zebrafish models for childhood neuromuscular disorders, providing a brief overview of results and the techniques, mainly transgenesis and chemical biology, used for genetic manipulation. The amount of data collected in the past few years will lead zebrafish to became a common functional tool for assessing rapidly drug efficacy and off-target effects in neuromuscular diseases and, furthermore, to shed light on new etiologies emerging from large-scale massive sequencing studies.

Gene selection and cancer type classification of diffuse large-B-cell lymphoma using a bivariate mixture model for two-species data

A bivariate mixture model utilizing information across two species was proposed to solve the fundamental problem of identifying differentially expressed genes in microarray experiments. The model utility was illustrated using a dog and human lymphoma data set prepared by a group of scientists in the College of Veterinary Medicine at North Carolina State University. A small number of genes were identified as being differentially expressed in both species and the human genes in this cluster serve as a good predictor for classifying diffuse large-B-cell lymphoma (DLBCL) patients into two subgroups, the germinal center B-cell-like diffuse large B-cell lymphoma and the activated B-cell-like diffuse large B-cell lymphoma. The number of human genes that were observed to be significantly differentially expressed (21) from the two-species analysis was very small compared to the number of human genes (190) identified with only one-species analysis (human data). The genes may be clinically relevant/important, as this small set achieved low misclassification rates of DLBCL subtypes. Additionally, the two subgroups defined by this cluster of human genes had significantly different survival functions, indicating that the stratification based on gene-expression profiling using the proposed mixture model provided improved insight into the clinical differences between the two cancer subtypes.

Mathematical Modeling of Alternative Polyadenylation in the Human Gene,CSTF3

A large number of human genes have been found to contain more than one polyadenylation site (poly(A) site). These lead to multiple messenger ribonucleic acid (mRNA) transcripts, although some of th...

Molecular profile of Treeshrew, a promising experimental animal for medical research

Scandentia order in Euarchontoglires consists of two families, Tupaiidae and Ptilocercidae , including five genera that contain 20 species. Genus Tupaia having 15 species is the largest genus in the order Scandentia . Most species in Scandentia have a karyotype 2n=52–68, therein, the well-known common treeshrew ( Tupaia glis ) has 2n=60; Northern treeshrew ( Tupaia belangeri chinensis , has 2n=62; pygmy treeshrew ( Tupaia minor ) has 2n=66 and mountain treeshrew ( Tupaia montana ) has 2=68, whereas only one species Mindanao treeshrew ( Urogaleeveretti ) has 2n=44. The whole genome Northern treeshrew ( Tupaia belangeri chinensis ) was sequenced and assembled recently. The size of a 2.86 GB genome was assembled that contains approximately 22 063 protein coding genes very closer to human gene number, and contains 35% of the repeat important element, and 14% of the dominated transposeon in the treeshrew genome. The functional annotation of some important genes and gene families will facilitate treeshrew becoming a promising experimental animal for medicine evaluation alternative to nonhuman primates.

Evolutionarily recent insertions of mobile elements and their contribution to human genome structure

Mobile elements are DNA fragments able to self-replicate in the genome of a host organism. Typically, mobile elements account for approximately 40–50% of the mammalian genome. This review summarizes the evolutionarily recent insertions of mobile elements that have taken place after the divergence of human and chimpanzee ancestral lineages, i.e., later than about 6 MYA. The human-specific mobile elements are represented by relatively small copy numbers and fall into the four following groups: HERV-K (HML-2), L1, Alu, and SVA. The amount of human-specific HERV-K (HML-2), L1, Alu, and SVA is about 150, 1200, 5500, and 860 copies per genome, respectively. In addition, we have succeeded in describing a new family of human-specific mobile elements, which are only present in the human genome and absent in the DNA of other primates. The insertions of human-specific mobile elements can be considered to be important candidates for the role of molecular genetic agents of anthropogenesis, since each new insertion of such a mobile element supplies an acceptor genomic locus with a set of new functional sites of transcription factor binding that are able to significantly contribute to the function of adjacent genes. The known facts that demonstrate the effect of human-specific mobile elements on the expression of neighboring genes allow the total number of human genes controlled by them to be estimated as several hundred.

Extensive Transcriptional Regulation of Chromatin Modifiers during Human Neurodevelopment

Epigenetic changes, including histone modifications or chromatin remodeling are regulated by a large number of human genes. We developed a strategy to study the coordinate regulation of such genes, and to compare different cell populations or tissues. A set of 150 genes, comprising different classes of epigenetic modifiers was compiled. This new tool was used initially to characterize changes during the differentiation of human embryonic stem cells (hESC) to central nervous system neuroectoderm progenitors (NEP). qPCR analysis showed that more than 60% of the examined transcripts were regulated, and >10% of them had a >5-fold increased expression. For comparison, we differentiated hESC to neural crest progenitors (NCP), a distinct peripheral nervous system progenitor population. Some epigenetic modifiers were regulated into the same direction in NEP and NCP, but also distinct differences were observed. For instance, the remodeling ATPase SMARCA2 was up-regulated >30-fold in NCP, while it remained unchanged in NEP; up-regulation of the ATP-dependent chromatin remodeler CHD7 was increased in NEP, while it was down-regulated in NCP. To compare the neural precursor profiles with those of mature neurons, we analyzed the epigenetic modifiers in human cortical tissue. This resulted in the identification of 30 regulations shared between all cell types, such as the histone methyltransferase SETD7. We also identified new markers for post-mitotic neurons, like the arginine methyl transferase PRMT8 and the methyl transferase EZH1. Our findings suggest a hitherto unexpected extent of regulation, and a cell type-dependent specificity of epigenetic modifiers in neurodifferentiation.

The role of microRNAs in glioma initiation and progression

micoRNAs (miRNAs) are small noncoding RNAs that regulate gene expression by targeting the mRNAs of a large number of human genes. Gliomas are the most common and deadly primary human brain tumors and are thought to originate from transformed stem-like cells (GSCs). microRNAs are frequently deregulated in cancer and gliomas and their deregulation has been associated with various aspects of glioma pathobiology. The present review summarizes the published literature on the role of miRNAs in gliomas with a focus on their role in GSCs.

Drawing the Map of Life inside the Human Genome Project (review)

Reviewed by: Drawing the Map of Life inside the Human Genome Project Nathaniel Comfort (bio) Drawing the Map of Life inside the Human Genome Project. By Victor McElheny. New York: Basic Books, 2010. Pp. 362. $28. The history of recent science is the second draft of history. That gives we who write it a special relationship to science reporters. We don’t have the luxury of dismissing them as unserious; often, their narratives are what those of us who work the leading edge of history must reinforce, revise, or refute. Since the 1970s Victor McElheny has chronicled the maturation of molecular biology from the thrilling vanguard of laboratory science into an economic powerhouse and the core discipline of biomedicine. His 2003 life of James Watson is the first biography of the celebrated co-solver of the structure of DNA. In his latest book McElheny draws on firsthand experience, news reports and press releases, interviews, the scientific literature, and some scholarly books in recounting the origins of the Human Genome Project and bringing its story up-to-date. He chooses to emphasize the genome as technology, an approach that, without some sophistication, easily leads to a triumphalist narrative—a seduction that McElheny makes no visible effort to resist. He begins, appropriately enough, in the 1970s, with the development of restriction enzymes, recombinant DNA, model organisms, and, of course, DNA sequencing. But then, inexplicably, he leaps to the 1993 identification of the Huntington’s disease gene—sometimes called the “crown jewel” of gene-hunting—before backtracking to deliver a quick briefing on the development of the biotechnology industry. With such balletic celebration McElheny flies past some critical techniques, such as human–mouse cell hybridization, invented by Mary Weiss and Howard Green and developed by Frank Ruddle and others, into the first effective means of mapping auto-somal human genes. Somatic cell genetics is not part of the canonical genome narrative. In fact, the entire narrative of clinical gene-mapping and the Human Genome Organization, so crucial to shaping the early genome project, is barely mentioned in this or other genome histories. McElheny is more interested in hitting the highlights than in conveying the richness of the history as it appeared while it was unfolding. The significant debate over whether to undertake a “big science” genome project is gathered under the rubric of “getting started.” If this book represents the historiographical trend, the disciplinary soul-searching of the late 1980s, so trenchantly covered by Robert Cook-Deegan in 1994 in The Gene Wars, is coming to be crammed into the prehistory of the genome. Perhaps it is becoming difficult, given the transformative effect of genomics on biology, to see that early dissent as much more than shortsightedness. Here, the project’s “crisis,” rather, comes in the late 1990s when Craig Venter turned the project on its head. Short-circuiting previous debates over which parts of the genome to sequence first and who had the most [End Page 240] expertise on which chromosome, Venter formed a private company and proposed to sequence the entire genome in one go. Or rather, a series of goes, cross-checked against one another to provide redundancy and therefore increased confidence. His approach telescoped the genome project from a ten-year slog into a mad three-year dash to a first draft of the genome in 2000. The second half of the book covers the fast-moving period since the turn of the century. This is the best part, since here the historiographical trail fades and one can easily feel lost in the jungle. Helpfully, McElheny roughs out many important moments of this dynamic, transitional period: the drastic downsizing of our estimates of the number of human genes; the surprising discovery of new and potent, though short-lived, forms of RNA; and the realization that the genome was far from a static “blueprint” or “parts manual.” It now seems a richly dynamic system, constantly rearranging itself and responding to the environment. The genome truly is, as Barbara McClintock said in 1980, a “sensitive organ of the cell.” This draft of history is quite rough, however. In the last, most valuable third, the narrative largely dissolves and the book becomes...

The human tripeptide GHK-Cu in prevention of oxidative stress and degenerative conditions of aging: implications for cognitive health.

Oxidative stress, disrupted copper homeostasis, and neuroinflammation due to overproduction of proinflammatory cytokines are considered leading causative factors in development of age-associated neurodegenerative conditions. Recently, a new mechanism of aging—detrimental epigenetic modifications—has emerged. Thus, compounds that possess antioxidant, anti-inflammatory activity as well as compounds capable of restoring copper balance and proper gene functioning may be able to prevent age-associated cognitive decline and ward off many common neurodegenerative conditions. The aim of this paper is to bring attention to a compound with a long history of safe use in wound healing and antiaging skin care. The human tripeptide GHK was discovered in 1973 as an activity in human albumin that caused old human liver tissue to synthesize proteins like younger tissue. It has high affinity for copper ions and easily forms a copper complex or GHK-Cu. In addition, GHK possesses a plethora of other regenerative and protective actions including antioxidant, anti-inflammatory, and wound healing properties. Recent studies revealed its ability to up- and downregulate a large number of human genes including those that are critical for neuronal development and maintenance. We propose GHK tripeptide as a possible therapeutic agent against age-associated neurodegeneration and cognitive decline.

LncRNAs: Finding the Forest Among the Trees?

One of the greatest surprises revealed when the first draft of the human genome was completed in 2003 was the total number of genes, which at ~20,500 fell well below even the most conservative of estimates.1 The numerous eukaryal genomes sequenced since then have continued to confound the common-sense notion that gene number and organismal complexity should be positively correlated, with examples such as the sponge and paramecium, both of whose gene numbers exceed that of humans. A corollary of the low human gene number is that the proportion of the genome that encodes protein, at just 2%, was also lower than expected, with the remainder largely discounted as nonfunctional, or “junk DNA.” In 2005, new light was shed on these noncoding regions of the genome when both large-scale complementary DNA sequencing and genome tiling arrays revealed that the majority of these areas were transcribed into RNA.2,3 These observations raised two fundamental questions: is the transcription of noncoding regions of the genome biologically meaningful, and could noncoding RNAs reconcile the apparent disparity between gene number and complexity? In a study reported recently in Nature, Guttman and colleagues took an important step toward answering these questions by demonstrating that knockdown of the vast majority of long noncoding RNAs (lncRNAs) expressed in embryonic stem (ES) cells affects gene expression patterns in a manner similar to that of knockdown of well-known ES cell regulators.4

Genome-wide evaluation and discovery of vertebrate A-to-I RNA editing sites

RNA editing by adenosine deamination, catalyzed by adenosine deaminases acting on RNA (ADAR), is a post-transcriptional modification that contributes to transcriptome and proteome diversity and is widespread in mammals. Here we administer a bioinformatics search strategy to the human and mouse genomes to explore the landscape of A-to-I RNA editing. In both organisms we find evidence for high excess of A/G-type discrepancies (inosine appears as a guanosine in cloned cDNA) at non-polymorphic, non-synonymous codon sites over other types of discrepancies, suggesting the existence of several thousand recoding editing sites in the human and mouse genomes. We experimentally validate recoding-type A-to-I RNA editing in a number of human genes with high scoring positions including the coatomer protein complex subunit alpha (COPA) as well as cyclin dependent kinase CDK13.

Recurrent chimeric RNAs enriched in human prostate cancer identified by deep sequencing

Transcription-induced chimeric RNAs, possessing sequences from different genes, are expected to increase the proteomic diversity through chimeric proteins or altered regulation. Despite their importance, few studies have focused on chimeric RNAs especially regarding their presence/roles in human cancers. By deep sequencing the transcriptome of 20 human prostate cancer and 10 matched benign prostate tissues, we obtained 1.3 billion sequence reads, which led to the identification of 2,369 chimeric RNA candidates. Chimeric RNAs occurred in significantly higher frequency in cancer than in matched benign samples. Experimental investigation of a selected 46 set led to the confirmation of 32 chimeric RNAs, of which 27 were highly recurrent and previously undescribed in prostate cancer. Importantly, a subset of these chimeras was present in prostate cancer cell lines, but not detectable in primary human prostate epithelium cells, implying their associations with cancer. These chimeras contain discernable 5' and 3' splice sites at the RNA junction, indicating that their formation is mediated by splicing. Their presence is also largely independent of the expression of parental genes, suggesting that other factors are involved in their production and regulation. One chimera, TMEM79-SMG5, is highly differentially expressed in human cancer samples and therefore a potential biomarker. The prevalence of chimeric RNAs may allow the limited number of human genes to encode a substantially larger number of RNAs and proteins, forming an additional layer of cellular complexity. Together, our results suggest that chimeric RNAs are widespread, and increased chimeric RNA events could represent a unique class of molecular alteration in cancer.

Abstract 3885: Inactivation of expression of many extremely large genes in oropharyngeal cancers

Abstract There are a number of human genes which span very large chromosomal regions. Forty genes span greater than 1 megabase and 200 are 500 Kb or larger. We and others have demonstrated that many of the largest genes are derived from within regions of profound genomic instability known as common fragile sites (CFSs). We have been studying oropharyngeal cancers which are derived from the base of tongue, tonsil and larynx. While the traditional etiologic factors underlying the development of this aggressive cancer is a history of smoking and drinking there are an increasing number of younger patients developing this cancer without these risk factors. The most likely cause of these cancers is the presence of human papillomavirus which we detect in over 90% of oropharyngeal cancers derived from the Mayo Clinic. In an attempt to better understand the molecular alterations that underlie oropharyngeal cancers arising from different risk factors we utilized the power of Next Generation sequencing on the Illumina GA IIx to compare the transcriptomes of 12 oropharyngeal cancers to patient matched normal tissue. We first observe a division of patients into two groups of oropharyngeal cancers: those caused by mutations and other alterations induced by a history of smoking and drinking and those associated with HPV infection caused by viral-induced genomic instability. We then examined the expression of the 200 largest human genes in the oropharyngeal tumors and find that each tumor has inactivated the expression of at least 20 different very large genes. There is a distinct pattern of inactivation of these genes in different oropharyngeal cancers depending upon the underlying etiology. Some of the genes most frequently inactivated include Dlg2 (the human homolog of the large discs tumor suppressor gene from drosophila and a mutation target in a number of other cancers); ERBB4 (Her4 and a member of the EGFR family), BAI3 (a brain specific angiogenesis inhibitor that is also mutated in multiple cancers), and ANK2 (mutated in long QT patients). Each of these genes may be functioning as tumor suppressors as has already been demonstrated for the two large CFS genes, FHIT and WWOX. The inactivation of so many of these genes in each oropharyngeal tumor may have a profound effect upon the phenotype of the resulting tumor. When we examine the expression of the large genes most frequently inactivated in each of the two groups of oropharyngeal cancers in panels of breast or lung cancer samples we find that we do not detect significant loss of expression of these genes. We believe that genomic instability promotes alterations in the unstable CFS regions but that there is selective inactivation of different large CFS genes in different cancers. The signature of which specific genes are inactivated may have phenotypic and clinical significance which we are just beginning to investigate. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3885. doi:10.1158/1538-7445.AM2011-3885

The functional spectrum of low-frequency coding variation

BackgroundRare coding variants constitute an important class of human genetic variation, but are underrepresented in current databases that are based on small population samples. Recent studies show that variants altering amino acid sequence and protein function are enriched at low variant allele frequency, 2 to 5%, but because of insufficient sample size it is not clear if the same trend holds for rare variants below 1% allele frequency.ResultsThe 1000 Genomes Exon Pilot Project has collected deep-coverage exon-capture data in roughly 1,000 human genes, for nearly 700 samples. Although medical whole-exome projects are currently afoot, this is still the deepest reported sampling of a large number of human genes with next-generation technologies. According to the goals of the 1000 Genomes Project, we created effective informatics pipelines to process and analyze the data, and discovered 12,758 exonic SNPs, 70% of them novel, and 74% below 1% allele frequency in the seven population samples we examined. Our analysis confirms that coding variants below 1% allele frequency show increased population-specificity and are enriched for functional variants.ConclusionsThis study represents a large step toward detecting and interpreting low frequency coding variation, clearly lays out technical steps for effective analysis of DNA capture data, and articulates functional and population properties of this important class of genetic variation.

The evolution of gene regulation, the RNA universe, and the vexed questions of artefact and noise

In the ten years since the first sequencing of the human genome, much has been made of the need to look to gene regulation, and not gene number or DNA sequence, for the evolution of organismal diversity and complexity - an issue that rose to prominence, with the realization first, that the number of human genes is about the same as the number required to specify a nematode worm; and second, that the DNA of H. sapiens is roughly 96% identical to that of the chimpanzee. But the realization that the secret of evolution lies in changes in gene regulation considerably predates the revela tions of genomics. Allan Wilson and colleagues, in a paper published in 1974 [1], drew attention to the simple and striking fact that morphologically homogeneous frog species also have relatively homogeneous karyo types, whereas mammalian species, which are marked ly diverse morphologically, also show major differ ences in chromosome number and organization; changes in proteins, by contrast, are much the same for both groups. They concluded that genome organization, and by implication gene regulation, is more important for metazoan evolution than protein sequence (and cite earlier publications of EB Ford and Susumu Ohno for the same insight). The following year, Mary-Claire King and Wilson published a more detailed examination of the chromosomal distinctions between human and chimpanzee [2], arguing compellingly, without benefit of highthroughput anything, that changes in the organization of the genome, and not changes in protein-coding sequence, must account for the crucial differences between the two primates. In those pre-genomic days, the protein data were in large part immunological and electrophoretic; the analysis of genome reorganization depended on chromosome banding patterns (Giemsa banding, not FISH); and almost nothing was known of the mechanism of gene regulation in eukaryotes. The ground between then and now is covered in a recent review by Sean Carroll [3], who acknowledges Emile Zuckerkandl and Eric Davidson as early proponents of the importance of gene regulation in morphological evolution and charts the remarkable history of the development of ideas consequent on the discovery of the homeobox genes, with a strong emphasis on the evolution of cis-regulatory elements - that is to say, DNA binding sites for gene regulatory proteins - as the basis for morphological change. The argument is that DNA regulatory elements and the proteins that bind to them, often combinatorially, constitute regulatory networks that can evolve rapidly through changes to the regulatory elements, which are often modular, different modules binding different proteins characteristic of distinct differentiated states of a cell. The gene regulatory proteins can also change, of course, but are generally more highly conserved than their binding sites. Tuch et al. [4] have published a short and pellucid overview of the essential points and principles of this schema, in the context of recent evidence on how such regulatory circuits can become rewired in yeast. Beyond regulatory proteins

Between a chicken and a grape: estimating the number of human genes.

The number of genes in the human genome is still an estimate.

Between a chicken and a grape: estimating the number of human genes

Between a chicken and a grape: estimating the number of human genes