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Sense and anti sense strand

Sense and anti sense strand


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Why the sense strand is only involved in transcription though the antisense strand just has the compliment strand of the sense strand?


The short answer is the transcription machinery will only bind on the correct orientation. The binding of proteins and such to the promoter DNA strand is determined by the sequence of the DNA, the sequence is not correct on the anti-sense strand for a given gene.


One of the reasons why DNA is double stranded--this means DNA has sense and antisense strands--is to make a copy.

During transcription, RNAs are transcribed referring to anti-sense strand sequences--making base pairs with anti-sense strand. In other words, the sense strand does not do anything during transcription.


Either strand of DNA can be sense or antisense. SWBarnes2 posts that the "transcription machinery will only bind on the correct orientation" and that is indeed what determines which strand is sense. But note his important statement "the sequence is not correct on the anti-sense strand FOR A GIVEN GENE" (my emphasis). As you move from gene to gene, the sense strand can swap strands. Coding sequences can overlap running in opposite directions, making both strands sense; this is more commonly a viral trick. Sense and antisense are defined by what sequence is found in RNA and so the map of sense and antisense strands on DNA is complicated. As you move along a strand of DNA one strand might be sense, then the other, then both, then neither.


In part (i), virtually all students identified the phosphate group.

Most were also able to identify the covalent or phosphodiester bond, although some stated it was an H bond.

This question was difficult for most students, although some wrote correct answers. In some scripts, students answered in terms of 3' &rarr 5', whereas others did not refer to the two strands, nor did they relate them to transcription.

Few students got full marks as they did not compare relative characteristics. For example, it appears that many candidates interpret "naked" DNA as not being within a nuclear envelope. With this assumption, it is more difficult for them to gain mark on correct pairs of statements.


What is Positive Sense RNA Virus

Positive sense RNA virus is a type of single-stranded RNA virus whose genetic material is viral mRNA that encodes for proteins. This means they contain the sense strand of RNA as their genome and it can be readily translated into proteins. Hence, positive sense RNA does not require an RNA polymerase packaged inside the virion. The 5’ end of the genome is either capped or naked while the 3’ end is polyadenylated or naked. Poliovirus, hepatitis C virus, dengue virus, SARS, West Nile virus, echovirus, and Coxsackie virus are examples of positive sense RNA viruses. An electron micrograph of hepatitis C virus is shown in figure 1.

Figure 1: Hepatitis C Virus

The replication of the positive sense RNA viruses occurs through the double-stranded RNA intermediate. Upon infection, the polyproteins encoded for the viral replication are translated. The replication of the single-stranded RNA leads to the formation of RNA duplex which in turn is transcribed into single-stranded positive genomic mRNA.


Is the antisense strand the same as the leading strand? DNA is confusing me.

They describe different things. Antisense just means it is the complementary sequence to some sequence/gene in question. Leading and lagging strands come into play during DNA replication.

Oh I see. But they refer to the same strand though but depending on which context. Thank you.

antisense strand is the strand complementary to the mrna sequence for a specific protein.

leading strand is the strand that is replicated at one go, unlike the lagging strand, which is replicated in okazaki fragments.

antisense strand concerns transcription and translation, while leading strand concerns dna replication.

right answer except that antisense refers to the strand that is not used as a template for transcription: it applies to all transcripts whether they are coding for a protein or not.

When you are referring to a specific Gene, the antisense strand is the template strand because RNA polymerase will use this strand to create an RNA molecule for the gene of interest. It is antisense because it is complementary to the RNA molecule that it was used to make. Leading and lagging strand are used to refer to strands of DNA when replication is taking place. It's a little confusing though because it's not really just one strand or the other that's leading or lagging. Its more like in certain spots of the DNA, it's zipped open and replication is happening faster on one strand and slower on the other. But in one spot the top strand can be lagging while another spot on the same strand would be leading.


Sense and antisense

Sense and antisense is part of the building blocks of the DNA double helix, base pairs contributes to the interior structure of RNA and DNA. In order to maintain the helical structure of the constant that is independent of the nucleotide sequence, the hydrogen bonds to allow the DNA strand, Watson – is determined by the specific pattern (thymine – – adenine and cytosine guanine) Crick base pairs. Complementary nature of the base pair structure provides a backup copy of all genetic information encoded in double-stranded DNA. Data redundancy and regular structure provided by the double helix DNA DNA, which has been made suitable for the storage of genetic information, base pairing received between nucleotides and DNA, the sequence of the DNA polymerase opposite strand is, I called “antisense” sequence. Different parts of the same strand of DNA (i.e., including the sense and antisense sequences to the two chains) sense and antisense sequences may be present in the. In prokaryotes and eukaryotes, to produce an antisense RNA sequence, RNA functions these are not entirely clear. One proposal is that it is involved in the regulation of gene expression through base pair RNA-RNA antisense RNA.

Sequences of prokaryotes and eukaryotes of DNA some more and more and a virus or plasmid, blurs the distinction between the sense and antisense strands by having a gene overlap. In these cases, the DNA sequences of several double duty encoding the protein molecules leading of one strand, and performs a second protein to be read in the opposite direction along the other strand. In bacteria, this overlap may be involved in the regulation of gene transcription while increasing the amount of information that can be viruses, gene duplication is encoded in a small viral genome.

The molecular biologist, call the chain (or plus (+)) of the DNA sense if the version of the same RNA sequence is translated into a protein or translated. The complementary strand antisense – called () or negative sense (). Phrase coding strand occurs occasionally, by transferring in both directions from the promoter region of the common some cases that encode non-coding RNA and protein also can be transcribed from both tracks, or two (see transcription following “ambisense” is an intron in the chain).

Complementary strand of two double-stranded DNA of (dsDNA) are separated as a chain “anti-sense” and usually, “sense” strand. In the sense strand, DNA is similar to the (mRNA) RNA, the human eye (e.g., ATG codon = methionine amino acid) may be used to read the protein code that is expected. However, DNA of the sense strand itself is not used for the preparation of proteins by the cell. This is an antisense DNA strand that serves as a source of protein source used as a template the base complementary DNA strand sense mRNA. Since the transfer results in a product of the RNA strand DNA template complementary mRNA, it is complementary to the antisense DNA strand. I used to (protein synthesis) translation of this mRNA.

Therefore, it is possible to cause the sense and antisense 5′-August 3 ‘base nucleotide triplet 3’-TAC-5 of the antisense strand of DNA “(methionine August codon, the start codon) in the triplet mRNA in use as a template The. distance sense DNA is, will have the ATG triplet that look exactly the same as in August, but not to be used to make mRNA, it is the effect of DNA strands. can not be used to methionine called “sense” is, as it is used, the protein is not a spiral, it is because having a sequence similar codon of the protein sequence.

If you do not understand the meaning of “meaning” They are, if you do not understand the complementarity, it might be confusing to students they. before the treaty is established, in order to further confusion, things are “nonsense” does not agree to the DNA strand, called “sense”, the oldest textbooks. In biological research, short antisense molecules may be reacted alter the expression of genes with a complementary strand of nucleic acid. Please see the following the “antisense oligonucleotide”.

DNA can be used to twist the rope in a process called DNA supercoiling. DNA and is a “relaxed” state, in the case of the DNA, twist strands become more tightly around the axis of the double helix, loosely wrapped once more usually every 10.4 base pairs chain. If it is twisted in the direction of the spiral, which is a positive supercoiling, DNA, is held tightly from each other bases. They are if you are twisted in the opposite direction, this is a super-coil negative, the base dissociate easily. In nature, DNA most is supercoiled slightly lower are introduced by an enzyme called topoisomerase. These enzymes are needed to relieve the torsional stress that was introduced into the DNA strand in the process of such transfer and replication of DNA.

Antisense RNA is a RNA transcript that is complementary to the endogenous mRNA. In other words, this is a non-coding strand, in addition to the coding sequence of RNA, which is the same as the negative sense RNA viruses. Introduction of a gene encoding antisense RNA is a technique that is used to block the expression of the gene. Antisense RNA is radioactively labeled may be used to display the transcription levels of genes in various cell types. The type of alternative part of the structure of the antisense, the antisense therapy at least one approved for use in humans treated antisense Related experimentally.

In forming a double stranded RNA and antisense sequences complementary, translation is blocked mRNA. This process is related to RNA interference. In order to prevent the expression of specific genes, antisense nucleic acid molecules can be used experimentally to bind to mRNA. Antisense therapy is under development in the U.S. Food and Drug Administration has approved phosphorothioate antisense oligo fomivirsen and (Vitravene) mipomersen the (Kynamro) for therapeutic use of human as well (FDA). Cells can be used to generate antisense RNA molecules that interact with mRNA molecules complementary naturally, to inhibit their expression. There is provided a mechanism for replicating the DNA, RNA polymerase transcription of DNA into RNA. DNA binding proteins, many can recognize a specific pattern of a pair of specific type specific regulatory region of the gene.

Intramolecular base pairing may occur in single-stranded nucleic acid. (E.g., AA or GU) to allow the various interactions of the click, Watson – – Non-Watson and formation of the double helical short chain This includes a (AS and GC) Crick base pairs, RNA molecules (e.g. , RNA is particularly important in transfer RNA), can be folded into a wide range of three-dimensional structure of a particular. Further, between messenger RNA base pairing transcribed RNA and the (tRNA) and (mRNA), as a result of the base sequence of mRNA underlying molecular recognition events, was translated into the amino acid sequence of the protein.

The DNA, because it is a double-stranded Generally, in many cases, the size of the entire genome of an organism or individual genes is measured in base pairs. Therefore, the number of base pairs in all is the number of nucleotides in (excluding non-coding region of one strand telomere) one of the wires. Estimates (23 chromosomes) long and about 3.2 billion base pairs in the haploid human genome, and contains the different genes from 25.000 to 20.000. Kilobases (KB) is a unit of molecular biology equal to 1000 base pairs of RNA or DNA.

In the double helix of DNA, each type of nucleic acid base of base 1 chain link on the only other circuits. This is called an auxiliary base pairs. Here, purines form hydrogen bonds thymine, adenine, pyrimidine gluing guanine cytosine bonded by hydrogen bonds only three hydrogen bonds and only two. This arrangement of two nucleotide binding, is called base pairs in the double helix. Hydrogen bond is not a covalent bond, it is possible to separate them, and recombine relatively easily. Both strands of the DNA double helix, you can zip by, or to open by high temperature and mechanical forces. As a result of this complementarity, all information in the helices of the two-stranded DNA sequence repeats every section is essential for DNA replication. Indeed, a specific interaction with this reversible, is important for all functions of DNA in living organisms between complementary base pairs.


Sense and anti sense strand - Biology

A DNA segment encoding a protein usually has a " sense " strand and a complementary " antisense " strand which acts as a template for RNA polymerase. Conventionally, the sense strand is considered to encode the protein since it has the same sequence as the mRNA. Attention has been drawn to the possibility of long open reading frames in the antisense strand which might encode " antisense " proteins (Meckler 1969 Biro 1981a,b Blalock and Smith 1984 Merino et al. 1994). Codons for hydrophilic and hydrophobic amino acids on the sense strand may sometimes be complemented, in frame, by codons for hydrophobic and hydrophilic amino acids on the antisense strand. Furthermore, antisense proteins may sometimes interact with high specificity with the corresponding sense proteins (Blalock and Bost 1986 Blalock 1990 Clarke and Blalock 1991). The interactions involve multiple contacts along the lengths of the polypeptide chains (Tropsha et al. 1992).

Yomo and coworkers (1992) interpreted the discovery of long antisense open reading frames in certain plasmid genes as indicating that some " unknown force " is protecting the frames from mutations generating stop codons. Recently, Yomo and Urabe (1994) have generalized these arguments taking into account the observation that the frequencies of individual codons in sense strands are often similar to their frequencies in the antisense strands (when read in the same phase and with the correct polarity Alff-Steinberger 1984, 1987 Yomo and Ohno 1989). Others have suggested that the genetic code may initially have evolved to favour the simultaneous emergence of sense and antisense peptides (Alff-Steinberger 1984 Zull & Smith 1990 Konecny et al. 1993).

The physiological relevance of antisense phenomena at the RNA level is well established (e.g. Tomizawa 1984). However, antisense phenomena at the protein level are more controversial (Goldstein and Brutlag 1989 Eberle and Huber 1991 Tropsha et al. 1992 Moser et al. 1993). I here point out that many antisense phenomena at the protein level can be interpreted as incidental by-products of

(i) the evolution of interactions between mRNA codons and tRNA anticodons (Eigen & Schuster 1978),

(ii) the fine-tuning of base composition to avoid inter species recombination ("GC/AT pressure" Filipsky 1990), and

(iii) the fine-tuning of stem-loop-forming potential to promote intra species recombination (" fold pressure " Forsdyke 1995b-d).

Non-Stop-Frames Use Same Frame as ORFs

A long open reading frame can only exist in the antisense strand if there are no stop codons. Following the convention of Yomo et al. (1992), I here refer to such frames as non-stop frames (NSFs), to distinguish them from the open reading frames (ORFs) of the sense strand.

From consideration of the context of interactions between codons and their cognate tRNA anticodons, it has been proposed that the modern genetic code evolved from a prototypic triplet code of general form RNY, where R is a purine base, N is any base, and Y is a pyrimidine base (Eigen and Schuster 1978 Bossi and Roth, 1980). Traces of this code seem to be present in some modern genes and may sometimes be used to predict ORFs (Shepherd 1982). Thus, to simplify, we may write a DNA sequence encoding a protein as a series of RNY codons.

Fig. 1 . The proposed prototypic triplet code (RNY) predicts a unique relationship between reading frames in sense and antisense strands of DNA. CSF1, CSF2, CSF3 refer to the three frames in the coding sense strand. CAF1, CAF2, CAF3 refer to the three corresponding frames in a coding antisense strand. Boxes with arrows indicate the polarity of coding triplets (5'--> 3').

Figure 1 shows this for the three frames in a coding sense strand (CSF1, CSF2, CSF3), and for the three corresponding frames in a coding antisense strand (CAF1, CAF2, CAF3). It is seen that the ORF designated CSF1 is the only frame in the sense strand which corresponds to RNY. Similarly, CAF1 is the only frame in the antisense strand which corresponds to RNY. Thus, an antisense NSF should usually be in the same frame as that of the corresponding ORF (Alff-Steinberger 1987). It can also be seen that CSF2 (NYR) corresponds to CAF3, not CAF2. Similarly, CSF3 (YRN) corresponds to CAF2, not CAF3. This was recently confirmed by Yomo and Urabe (1994) in a study of long codon sets generated by combining E. coli coding regions into one long sequence. Thus their results are consistent with the proposal of a prototypic RNY code, as well as with the existence of genes in the antisense strand (as they suggest).

If there are no stop codons (TAG, TAA, TGA) in the NSF, then there can be no complementary codons (CTA, TTA, TCA) in the corresponding ORF. CTA and TTA code for leucine. TCA codes for serine. These two amino acids are found frequently in proteins. Thus, except for an unlikely ORF with no leucine or serine, whether there will be a long NSF depends on which synonymous codons for leucine and serine are used in the corresponding ORF. Leucine and serine are two of the three amino acids for which there are six synonymous codons. An important factor determining codon choice is the species-specific pressure on a genome to adopt a particular (G+C)% base composition ("GC/AT pressure" reviewed by Filipski 1990). AT-rich codons are used infrequently in species with a high (G+C)% (i.e. RNY is usually GNC).

In Figure 2a the combined average frequencies of the usages of CTA, TTA and TCA as codons in sets of genes from various species are plotted against the corresponding average percentages of G+C in coding regions calculated from the frequency and GC content of all the codons of each gene set. The latter should provide a measure of GC/AT pressure. The data are taken from the species codon usage profiles of Wada et al. (1990). The right ordinate shows the average length of NSF expected at particular values of the usage of CTA, TTA and TCA. Thus 1% usage of the codons implies an average NSF of 100 codons. An extreme example is Rhodobacter capsulatum (RCA) which uses CTA, TTA and TCA at a frequency of only 0.05%, implying an average NSF of 2000 codons in the 21 genes examined by Wada et al. (1990).

Fig. 2 . Potential length of open reading frames in the antisense strand (NSF) increases as (G+C)% of total codons increases. Codon usage tables for various species were used to calculate the sum of the frequencies of (a) the codons CTA, TTA and TCA, which are the complements of stop codons (TAG, TAA, TGA), and (b) the codons GTA and ATA, which are members of the set of codons of general form NTA. From knowledge of the frequency and GC content of individual codons, the overall GC content of the coding regions used to construct the tables were also calculated (abscissa). Data-points for individual species are shown as filled circles. Data-points for plasmid genes encoding enzymes which degrade nylon oligomers are shown as triangles.

As the (G+C)% increases, preferred codons become increasingly GC-rich, and the combined usage of the AT-rich codons CTA, TTA and TCA decreases. It was found empirically that there is an approximately rectilinear relationship between the logarithm of the sum of the percentages of CTA, TTA and TCA, and the average (G+C)% of the corresponding coding regions. However, at high G+C percentages, values for the frequency of CTA+TTA+TCA for two species, Azotobacter vinelandii (AVI) and Rhodobacter capsulatus, are below the lower limit of the 95% prediction interval (estimated using Minitab statistics software Ryan and Joiner 1994). TCA participates equally with CTA and TTA in decreasing in frequency disproportionately at high (G+C)% in these species. A species with more GC-rich codons, Streptomyces (STM), remains close to the regression line.

The divergence is also apparent in the case of GC-rich plasmid genes (shown as triangles), which encode bacterial nylon-degrading enzymes (Yomo, Urabe and Okada 1992). Except for the gene NA26AHDH, the values for the sum of the percentages of CTA+TTA+TCA as codons in these genes are zero (corresponding to a completely open average NSF). The value for NA26AHDH is close to the regression line and corresponds to an average NSF of 400 codons. However, the difference between NA26AHDH and the other plasmid genes is due to only one codon (TCA is present once in NA26AHDH). In a series of only four genes this difference is not statistically significant, so does not support the suggestion that there is some special mechanism protecting the plasmid NSFs from accumulating mutations that generate stop codons (Yomo et al 19921994). Such a special mechanism might be expected to affect only CTA, TTA and TCA. However, in the plasmids there are zero frequencies not only of these codons, but also of seven of the eight codons of general formula W3 (e.g. TTT, ATA, etc.), and of about half the 24 codons of general formula W2S (e.g. AGA, TGT, etc.). It seems likely that, as suggested by Ikehara and Okazawa (1993), the plasmid genes are merely responding to GC/AT pressure, and not to some " unknown force ".

Assuming that the observed regression line (Fig. 2a) is a close representation of the relationship between GC/AT pressure and the frequencies of CTA+TTA+TCA, then species whose frequencies of these codons fall close to the regression line would appear to be responding simply to GC/AT pressure. The species whose frequencies of the codons diverge significantly below the line at high GC/AT pressures would lend some credence to the " unknown force " postulate.

The average NSF for all the 37 genes of Azotobacter vinelandii, and for all the 21 genes of Rhodobacter capsulatus (that were studied by Wada et al. 1990), is greater than predicted by the regression line. The " unknown force " would seem to have acted on all the genes of these species. It would seem unlikely that all 58 genes would have sufficient flexibility in the coding of the sense strand product to permit the evolution of a useful antisense strand product. Thus, either pressures to form each antisense protein have not been causing these genes to loose CTA, TTA and TCA, or the only way pressure to form antisense protein can work is by committing numerous " innocent bystander " genes to the same strategy that is, the evolution of one particular antisense product was so advantageous that all the genes in the organism were required to respond to some " unknown force " in order to acquire the potential to generate an antisense product. Alternatively, the organisms could be responding to some intrinsic species specific " unknown force " the blind consequences of which would be NSFs longer than predicted from (G+C)%.

Role for TpA Pressure in Rhodobacter?

In Rhodobacter capsulatus two codons of general form NTA (CTA and TTA) have zero frequency, and TCA has a frequency of 0.05%. The latter value is the lowest of all the species tabulated by Wada et al. (1990), except for Azotobacter vinelandii (0.01%). The low values are not specific to these three codons. Figure 2b, shows plots of the combined frequencies of two other codons of general form NTA (GTA, encoding valine ATA, encoding isoleucine). As in Figure 2a, most of the data-points are close to the regression line. The point corresponding to Rhodobacter capsulatus diverges below the regression line. Indeed in this species the usage of GTA + ATA is zero, which is beyond the 95% prediction interval (Ryan and Joiner 1994). Thus, it is possible that the divergence may be ascribed, in part, to " TpA pressure ", which is a " known " but not well understood pressure (Nussinov 1984 Alff-Steinberger, 1987 Barrai et al. 1991). TpA pressure affects all codons of general forms NTA and TAN (Forsdyke, 1995d).

The point corresponding to Azotobacter vinelandii is closer to the regression line and is within the 95% prediction interval. In this species the average usages of GTA and ATA are 0.27% and 0.06% respectively. With respect to these codons this organism may simply be responding to GC/AT pressure. Thus TpA pressure does not appear to explain the low levels of CTA and TTA in Azotobacter vinelandii. Here the " unknown force " postulate may be valid.

Similar Codon Frequencies in Sense and Antisense Strands

Sense and antisense strands have similar codon frequencies in various organisms (Alff-Steinberger 1984, 1987). Furthermore, trinucleotides with the potential to encode hydrophilic amino acids (e.g. GAA glutamate), are present at approximately the same frequencies as their complements, which often have the potential to encode hydrophobic amino acids (e.g. UUC phenylalanine). However, studies of the frequencies of dinucleotides (Nussinov 1984), trinucleotides (Yomo and Ohno 1989 Ohno and Yomo 1991), and higher oligonucleotides (Pradhu 1993), show this to be a general characteristic of DNA sequences, both coding and in non-coding.

One explanation for this, proposed by Nussinov (1982), was that DNA might contain numerous inverted repeats. These would confer on DNA the ability to form stem-loop, cruciform, structures. Indeed, evidence obtained by comparing the optimum folded structures of " windows " in natural sequences with the optimum folded structures of the same windows in which the order of bases have been randomized, suggests that all DNA sequences have been under an evolutionary selection pressure to maximize the ability to form local stem-loop structures (" fold pressure "). This affects both protein-coding and non-coding regions (introns and intergenic regions Forsdyke 1995b,c).

Fig. 3 . If there are palindromes in exons then there is a potential for sense and antisense proteins to have motifs in common. Upper: Codons in duplex DNA, which has adopted cruciform configurations, are shown as arrow-headed boxes, as in Figure 1. Codons which complement each other to form the stems of stem-loops are shown within boxes. The amino acids corresponding to each codon are shown in bold lettering. Lower: Amino acid sequence of the sense and antisense proteins derived from the above DNA sequence. Amino acids in boxes represent motifs present in both sequences.

The automatic consequence of this for protein sequences has been pointed out by Ohno and Yomo (1991), and is illustrated in Figure 3. Some motifs present in sense strand-derived proteins will also be present on the antisense strand-derived proteins. Thus, the properties of the latter may include some of those of the former. Since under appropriate conditions proteins can be induced to self-aggregate (Lauffer 1975 Forsdyke 1994, 1995a), there is the possibility of reaction of sense-strand derived proteins with the corresponding " near-self " proteins encoded by antisense strands. Should this or any other property of the antisense protein prove advantageous, then there would be the possibility of further evolutionary selection, which might result in further modification both of sense and antisense-derived proteins. However, for this opportunity to arise two prior evolutionary forces are likely to have acted. First, GC-pressure should have modified the genome such that long NSFs were feasible. Secondly, fold pressure should have attained equilibrium with other selective forces acting on the protein. As discussed elsewhere (Forsdyke 1995b), a section of DNA encoding a protein can adapt to fold pressure either by

  • (i) adopting an appropriate synonymous codon, or
  • (ii) allowing a conservative amino acid change, or by
  • (iii) encoding the protein in discrete units (exons) interrupted by sequences where stem-loop potential is less restrained (introns).

Acknowledgements. I thank D. Bray of Queen's University StatLab for advice, and I. Chaiken for assistance in tracing the early antisense literature. The work was supported by a grant from the Medical Research Council of Canada.

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Sense-antisense miRNA pairs constitute an elaborate reciprocal regulatory circuit

Antisense transcription of protein-coding genes has been increasingly recognized as an important regulatory mechanism of gene expression. However, less is known about the extent and importance of antisense transcription of noncoding genes. Here, we investigate the breadth and dynamics of antisense transcription of miRNAs, a class of important noncoding RNAs. Because the antisense transcript of a miRNA is likely to form a hairpin suitable as the substrate of ADARs, which convert adenosine to inosine in double-stranded RNAs, we used A-to-I RNA editing as ultrasensitive readout for antisense transcription of the miRNAs. Through examining the unstranded targeted RNA-seq libraries covering all miRNA loci in 25 types of human tissues, we identified 7275 editing events located in 81% of the antisense strand of the miRNA loci, thus uncovering the previously unknown prevalent antisense transcription of the miRNAs. We found that antisense transcripts are tightly regulated, and a substantial fraction of miRNAs and their antisense transcripts are coexpressed. Sense miRNAs have been shown to down-regulate the coexpressed antisense transcripts, whereas the act of antisense transcription, rather than the transcripts themselves, regulates the expression of sense miRNAs. RNA editing tends to decrease the miRNA accessibility of the antisense transcripts, therefore protecting them from being degraded by the sense-mature miRNAs. Altogether, our study reveals the landscape of antisense transcription and editing of miRNAs, as well as a previously unknown reciprocal regulatory circuit of sense-antisense miRNA pairs.

© 2020 Song et al. Published by Cold Spring Harbor Laboratory Press.

Figures

Extensive editing of miRNA-ATs. (…

Extensive editing of miRNA-ATs. ( A ) Schematic of miRNA-AT identification via A-to-I…

The characterization of miRNA-ATs. (…

The characterization of miRNA-ATs. ( A ) Comparison of the number of miRNA-ATs…

miRNAs regulate the expression of…

miRNAs regulate the expression of miRNA-ATs. ( A ) Annotation of the regions…

RNA editing modulates miRNA-mediated regulation…

RNA editing modulates miRNA-mediated regulation of miRNA-ATs. ( A ) The percentage of…

Global pattern of expression of…

Global pattern of expression of sense–antisense miRNA pairs. ( A ) Schematic representation…

The act of antisense transcription,…

The act of antisense transcription, rather than the transcripts themselves, regulates the expression…

Schematic model of the regulatory…

Schematic model of the regulatory network of sense–antisense miRNA pairs. In a cell,…


Sense and antisense direction - final explanation - Let solve this finally! (Oct/02/2007 )

I would be pleased if someone with experience can help me in solving the problem regarding direction of reading of plasmid in order to get sense and antisense RNA probe for in situ RNA hybridization.

I am confused as I got two completely opposite answers from two molecular biologists. So, question is: how do I know which sequence I use for sense and which for antisense production. Take this example: I know orientation of my insert and I will use polymerase (T7, Sp6, or whatever, depending of plasmid) in the direction in which is exactly sense strand of DNA (+/+). Do I get senseRNA or antisenseRNA probe? Two mol. biologists confused me: one told me that plasmid DNA is recognized as any other DNA, in other words, if polymerase reads template (not sense) strand, than I would expect that reading in sense DNA direction produces senseRNA. However, I got information that in this commercial plasmids it is just opposite: one should understand that polymerase reads exactly the cloned strand (not template), so sense strand produces antisenseRNA. To make things even more complicated, one biologists told me that DNA during cloning can make flip/flop movement, so, sense and antisense can exchange places "laterally". (how is that possible? DNA should know which is 5 and which is 3 end?!). Theoretically, one could test that only by sequencing (as restriction enzymes cut both strands and this do not change orientation of cloned DNA).

well i think both are quite right, even if i don't figured it out completely.
The plasmid point of view tells you what is sense and antisense, according to gene nomenclature.

In commercial kit, i think it's mentionned antisense to figure that the probe you construct is perfectly annealing with the RNA you want to probe. So in this point of view, your probe is an antisense probe.

Well, let's start the with RNA rather than the DNA. Sense RNA is RNA which can be translated into protein by ribosomes. It has a 5' AUG codon and a 3' UAA, UGA, or UAG stop codon. There is no ambiguity about this.

Confusion starts with the DNA. A promoter makes a sense piece of RNA by copying a DNA strand which is its reverse complement. This is sometimes called the template strand. But if you are starting at the promoter and reading left to right, this template strand will the reverse complement of the sequence you normally read. I don't care what you call the two strands of DNA, but the one you normally read starting at the promoter is the same (except for the T->U difference) as the RNA strand. Now this strand is not the one which is actually used to produce the RNA (that is, it is not the template) but it is the one which is normally thought about. It will include a start codon ATG at the 5' end, and a stop codon TAA, TGA or TAG at the 3' end.

Thank you for answers, but one can still be confused. Lets take an example: sequence which I want to detect using in situ RNA hybridization is ATC TAG. This is, of course, ++ strand of the gene. I clone this in the plasmid, check orientation and now I know that on the "left" side of it I have T3 polymerase and on the "right" T7. In other words, T3 will go from A to G in my sequence and T7 goes in an opposite direction. BUT! Does T3 polymerase read "ATC TAG", making TAG ATC or it reads template of it, making "ATC TAG" (as in "normal", eucariotic cells). In the first case, I will get "antisense riboprobe" and in another "sense riboprobe"!
So, which polymerase gives sense and which antisense in this very example?

So, here is your plasmid:
5' <T3 promoter ----> ATCTAG <---- reverse complement of T7 promoter> 3'

The T3 promoter will make the RNA molecule 5' AUCUAG 3'. The T7 promoter will make the molecule 5' CUAGAU 3'. To detect the RNA sequence 5' AUCUAG 3' which I gather is what you want to do, you need the molecule 5' CUAGAU 3'. made from the T7 promoter, since this is the one which will hybridize with your desired target.

So, here is your plasmid:
5' <T3 promoter ----> ATCTAG <---- reverse complement of T7 promoter> 3'

The T3 promoter will make the RNA molecule 5' AUCUAG 3'. The T7 promoter will make the molecule 5' CUAGAU 3'. To detect the RNA sequence 5' AUCUAG 3' which I gather is what you want to do, you need the molecule 5' CUAGAU 3'. made from the T7 promoter, since this is the one which will hybridize with your desired target.

Thank you very much. I got this answer from two sources and that was my opinion, too. Now I will take this as a rule.


Sense-antisense (complementary) peptide interactions and the proteomic code potential opportunities in biology and pharmaceutical science

Introduction: A sense peptide can be defined as a peptide whose sequence is coded by the nucleotide sequence (read 5' → 3') of the sense (positive) strand of DNA. Conversely, an antisense (complementary) peptide is coded by the corresponding nucleotide sequence (read 5' → 3') of the antisense (negative) strand of DNA. Research has been accumulating steadily to suggest that sense peptides are capable of specific interactions with their corresponding antisense peptides. Unfortunately, although more and more examples of specific sense-antisense peptide interactions are emerging, the very idea of such interactions does not conform to standard biology dogma and so there remains a sizeable challenge to lift this concept from being perceived as a peripheral phenomenon if not worse, into becoming part of the scientific mainstream.

Areas covered: Specific interactions have now been exploited for the inhibition of number of widely different protein-protein and protein-receptor interactions in vitro and in vivo. Further, antisense peptides have also been used to induce the production of antibodies targeted to specific receptors or else the production of anti-idiotypic antibodies targeted against auto-antibodies. Such illustrations of utility would seem to suggest that observed sense-antisense peptide interactions are not just the consequence of a sequence of coincidental 'lucky-hits'. Indeed, at the very least, one might conclude that sense-antisense peptide interactions represent a potentially new and different source of leads for drug discovery. But could there be more to come from studies in this area?

Expert opinion: Studies on the potential mechanism of sense-antisense peptide interactions suggest that interactions may be driven by amino acid residue interactions specified from the genetic code. If so, such specified amino acid residue interactions could form the basis for an even wider amino acid residue interaction code (proteomic code) that links gene sequences to actual protein structure and function, even entire genomes to entire proteomes. The possibility that such a proteomic code should exist is discussed. So too the potential implications for biology and pharmaceutical science are also discussed were such a code to exist.

Keywords: antisense peptide genetic code peptide–peptide interactions peptide–protein interactions proteomic code sense peptide.


Sense and anti sense strand - Biology

Will a mutation on the SENSE strand changes anything? During replication, it is only the ANTI-sense strand is transcribed.

Answered By Dr. Amandeep T

A mutation in the "sense" strand will affect the next generation if its in the "sense" strand of the DNA of germ cells, given the situation that the mutation does not get repaired by the DNA repair mechanisms of that cell.

Answered By Leora C

To add to Dr. Amandeep&rsquos answer, yes, it could change things. It would be dependent upon which cells the mutation occurred in. If the mutation occurred in a germ cell, and wasn&rsquot repaired, a mutation would show up in both the sense and anti-sense strands as that DNA is replicated due to the strands needing to form chemical bonds with one another. Even though the anti-sense strand is being transcribed, it must match up with the nucleotides of the sense strand. What would also matter would be if the DNA in question is in a coding region of the DNA (exon).

Answered By Manasa R

In basic transcription, not ocnsidering anythign else, the mutation to the sense strand wont change anything, a mutation to the anti-sense strand definetly would change it because it would affect the amino acid that would pair with it (codon).

Answered By manjula b

LET US BEGIN WITH AN EXAMPLE OF MUTATION IN SENSE STRAND OF DNA , IF A SPELLING ERROR OCCURS (GCA &ndashGCT) IN WHICH AN &ldquoA&rdquo IS REPLACED BY AT IN THS SENSE STRAND , CAUSING COMPLEMETERY CHANGES IN THE ANTISENSE DNA STRAND ALSO.( CGT &ndashCGA)

DURING TRANSCRIPTION m RNA CHANGES FROM GCA TO GCU.

BUT NO CHANCES OCCUR IN THE AMINO ACID BECAUSE OF THE INHERENT REDUNDANCY IN DNA CODE.

SO , ITS ALL DEPEND UPON THE TYPE OF CELL WHERE IN THE MUTATION TAKES PLACE : SOMATIC OR GERM CELL .

MOST SOMATIC CELL MUTATION HAVE NO PRACTICLE IMPACT ON THE ORGANISM.

IF MUTATION TAKES PLACE IN GERM CELL THAT IS FERTILIZED , THE MUTATION IS PRESENT IN ALL THE CELLS OF THE OFFSPRING AND WELL PASSED ON TO THE NEXT GENERATION.

Answered By manjula b

LET US BEGIN WITH AN EXAMPLE OF MUTATION IN SENSE STRAND OF DNA , IF A SPELLING ERROR OCCURS (GCA &ndashGCT) IN WHICH AN &ldquoA&rdquo IS REPLACED BY "T" IN THS SENSE STRAND , CAUSING COMPLEMETERY CHANGES IN THE ANTISENSE DNA STRAND ALSO.( CGT &ndashCGA)

DURING TRANSCRIPTION m RNA CHANGES FROM GCA TO GCU.

BUT NO CHANCES OCCUR IN THE AMINO ACID BECAUSE OF THE INHERENT REDUNDANCY IN DNA CODE.

SO , ITS ALL DEPEND UPON THE TYPE OF CELL WHERE IN THE MUTATION TAKES PLACE : SOMATIC OR GERM CELL .

MOST SOMATIC CELL MUTATION HAVE NO PRACTICLE IMPACT ON THE ORGANISM.

IF MUTATION TAKES PLACE IN GERM CELL THAT IS FERTILIZED , THE MUTATION IS PRESENT IN ALL THE CELLS OF THE OFFSPRING AND WELL PASSED ON TO THE NEXT GENERATION.



Comments:

  1. Wethrleah

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