Discussion of all aspects of biological molecules, biochemical processes and laboratory procedures in the field.
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If sDNA loses a base sequence there is no way to find that sequence. Whereas if a dDNA loses a base, the complementary sequence can be found because there's one complementary base. Ideally, if an organism evolves a quadruple redundant DNA structure, it would be able to withstand ageing, radiation etc...
Does this double stranded form help conserve the genetic material ? I think, yes, & this wud have been important pt. in earlier environment ..
& what about RNA to DNA change over ? Is there any special benefit of DNA over RNA ?
Thanks. , but this is what we see today . Actually RNA was genetic material before DNA as per the "RNA world hypothesis". Then , I think , at that time RNAs wud be larger than those we see today, so this doesn't seem to be the reasone. Further , smaller size of RNA is advantagious from communication pt. of view , so this may explain why RNA acts as communicator but this cannot explain the RNA to DNA change over as equal lengths of DNA & RNA will have equal no. of information , I think, we cannot say that DNA is larger so it can store more info.
By saying RNA to DNA change over I mean appearance of T instead of U in the genetic material.So, i want to know if there are any advantages of T over U.....
I don't know. A possibility is that RNA has a 4' OH group. This group should be both more reactive than the 4' H in DNA as well as a source of hydrogen bonding effects.
-Yes, It is also a stabilizing factor. Thanx .
But,-- Sugars in -NAs don't participate in H-bonding.
This article from Virology Journal (http://www.virologyj.com/home) might be of interest to the readership as it (among other things) describes a mechanism that enables protein information to modify RNA information, and is a mechanism of Larmarkian inheritance. The author makes it clear that it remains consistent with Darwinian selection. It also suggest potential weaknesses in viral replication that might be exploited.
Hepatitis C (HCV), hepatitis B (HBV), the human immunodeficiency viruses (HIV), and other viruses that replicate via RNA intermediaries, cause an enormous burden of disease and premature death worldwide. These viruses circulate within infected hosts as vast populations of closely related, but genetically diverse, molecules known as "quasispecies". The mechanism(s) by which this extreme genetic and antigenic diversity is stably maintained are unclear, but are fundamental to understanding viral persistence and pathobiology. The persistence of HCV, an RNA virus, is especially problematic and HCV stability, maintained despite rapid genomic mutation, is highly paradoxical. This paper presents the hypothesis, and evidence, that viruses capable of persistent infection autoregulate replication and the likely mechanism mediating autoregulation--Replicative Homeostasis--is described. Replicative homeostasis causes formation of stable, but highly reactive, equilibria that drive quasispecies expansion and generates escape mutation. Replicative homeostasis explains both viral kinetics and the enigma of RNA quasispecies stability and provides a rational, mechanistic basis for all observed viral behaviours and host responses. More importantly, this paradigm has specific therapeutic implication and defines, precisely, new approaches to antiviral therapy. Replicative homeostasis may also modulate cellular gene expression.
9 posts • Page 1 of 1
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