arXiv subjects

Erez Y. Levanon

Publications and source records attributed to Erez Y. Levanon.

8 recordsLinked to original sources

arXiv2006

Connectivity and expression in protein networks: Proteins in a complex are uniformly expressed

We explore the interplay between the protein-protein interactions network and the expression of the interacting proteins. It is shown that interacting proteins are expressed in significantly more similar cellular concentrations. This is largely due to interacting pairs which are part of protein complexes. We solve a generic model of complex formation and show explicitly that complexes form most efficiently when their members have roughly the same concentrations. Therefore, the observed similarity in interacting protein concentrations could be attributed to optimization for efficiency of complex formation.

q-bio.MN↗

arXiv2005

Is there any sense in antisense editing?

A number of recent studies have hypothesized that sense-antisense RNA transcript pairs create dsRNA duplexes that undergo extensive A-to-I RNA editing. Here we studied human and mouse genomic antisense regions, and found that the editing level in these areas is negligible. This observation puts in question the scope of sense-antisense duplexes formation in-vivo, which is the basis for a number of proposed regulatory mechanisms.

q-bio.GN↗

arXiv2005

Evidence for abundant transcription of non-coding regions in the Saccharomyces cerevisiae genome

Background: Recent studies in a growing number of organisms have yielded accumulating evidence that a significant portion of the non-coding region in the genome is transcribed. We address this issue in the yeast Saccharomyces cerevisiae. Results: Taking into account the absence of a significantly large yeast EST database, we use microarray expression data collected for genomic regions erroneously believed to be coding to study the expression pattern of non-coding regions in the Saccharomyces cerevisiae genome. We find that at least 164 out of 589 (28%) such regions are expressed under specific biological conditions. In particular, looking at the probes that are located opposing other known genes at the same genomic locus, we find that 88 out of 341 (26%) of these genes support antisense transcription. The expression patterns of these antisense genes are positively correlated. We validate these results using RT-PCR on a sample of 6 non-coding transcripts. Conclusions: 1. The yeast genome is transcribed on a scale larger than previously assumed. 2. Correlated transcription of antisense genes is abundant in the yeast genome. 3. Antisense genes in yeast are non-coding.

q-bio.GN↗

arXiv2005

Evolutionarily conserved human targets of adenosine to inosine RNA editing

A-to-I RNA editing by ADARs is a post-transcriptional mechanism for expanding the proteomic repertoire. Genetic recoding by editing was so far observed for only a few mammalian RNAs that are predominantly expressed in nervous tissues. However, as these editing targets fail to explain the broad and severe phenotypes of ADAR1 knockout mice, additional targets for editing by ADARs were always expected. Using comparative genomics and expressed sequence analysis, we identified and experimentally verified four additional candidate human substrates for ADAR-mediated editing: FLNA, BLCAP, CYFIP2 and IGFBP7. Additionally, editing of three of these substrates was verified in the mouse while two of them were validated in chicken. Interestingly, none of these substrates encodes a receptor protein but two of them are strongly expressed in the CNS and seem important for proper nervous system function. The editing pattern observed suggests that some of the affected proteins might have altered physiological properties leaving the possibility that they can be related to the phenotypes of ADAR1 knockout mice.

q-bio.GN↗

arXiv2004

Is abundant A-to-I RNA editing primate-specific?

A-To-I RNA editing is common to all eukaryotes, associated with various neurological functions. Recently, A-to-I editing was found to occur abundantly in the human transcriptome. Here we show that the frequency of A-to-I editing in humans is at least an order of magnitude higher as that of mouse, rat, chicken or fly. The extraordinary frequency of RNA editing in human is explained by the dominance of the primate-specific Alu element in the human transcriptome, which increases the number of double-stranded RNA substrates.

q-bio.GN↗

arXiv2004

Systematic identification of abundant A-to-I editing sites in the human transcriptome

RNA editing by members of the double-stranded RNA-specific ADAR family leads to site-specific conversion of adenosine to inosine (A-to-I) in precursor messenger RNAs. Editing by ADARs is believed to occur in all metazoa, and is essential for mammalian development. Currently, only a limited number of human ADAR substrates are known, while indirect evidence suggests a substantial fraction of all pre-mRNAs being affected. Here we describe a computational search for ADAR editing sites in the human transcriptome, using millions of available expressed sequences. 12,723 A-to-I editing sites were mapped in 1,637 different genes, with an estimated accuracy of 95%, raising the number of known editing sites by two orders of magnitude. We experimentally validated our method by verifying the occurrence of editing in 26 novel substrates. A-to-I editing in humans primarily occurs in non-coding regions of the RNA, typically in Alu repeats. Analysis of the large set of editing sites indicates the role of editing in controlling dsRNA stability.

q-bio.GN↗

arXiv2003

Human housekeeping genes are compact

We identify a set of 575 human genes that are expressed in all conditions tested in a publicly available database of microarray results. Based on this common occurrence, the set is expected to be rich in "housekeeping" genes, showing constitutive expression in all tissues. We compare selected aspects of their genomic structure with a set of background genes. We find that the introns, untranslated regions and coding sequences of the housekeeping genes are shorter, indicating a selection for compactness in these genes.

q-bio.GN↗

arXiv2003

Preferential attachment in the protein network evolution

The Saccharomyces cerevisiae protein-protein interaction map, as well as many natural and man-made networks, shares the scale-free topology. The preferential attachment model was suggested as a generic network evolution model that yields this universal topology. However, it is not clear that the model assumptions hold for the protein interaction network. Using a cross genome comparison we show that (a) the older a protein, the better connected it is, and (b) The number of interactions a protein gains during its evolution is proportional to its connectivity. Therefore, preferential attachment governs the protein network evolution. The evolutionary mechanism leading to such preference and some implications are discussed.

cond-mat.stat-mech↗