Are long non-coding RNAs (lncRNA) the missing “lnc” to revive Lamarck’s idea of inheritance of acquired characteristics?
Maybe so, in part. Thus claims an article by Kevin Morris in The Scientist. The old giraffe story may be wrong (baby giraffe inherits long neck from father’s stretching), but there are epigenetic mechanisms at work that appear to create heritable changes in response to the environment. One of them is the work of long, non-coding RNAs (lncRNA). These are RNA transcripts of non-coding DNA. Some of them can be thousands of base pairs long. Estimates put them at 70% to 98% of all transcripts present in the cell.
Once considered “junk DNA” (or “junk RNA”), lncRNA’s are now garnering more scientific attention on the assumption that the cell wouldn’t waste so much energy transcribing the DNA into these transcripts unless there was a purpose. Notice Morris’s design reasoning:

While epigenetic modifications to the genome are well studied, far less is known about how particular epigenetic marks are directed to their target loci. Clearly, something is guiding the modifications, which appear to be differentially distributed based on particular stresses induced on the cell or organism. Recent studies suggest that epigenetic changes, and possibly transgenerational epigenetic inheritance, could be explained by a somewhat unexpected molecular player: long noncoding RNA. (Emphasis added.)

Let’s follow along on a lncRNA to try to determine what it does. When a new transcript emerges from the replication fork, our lncRNA immediately binds to it, thus rendering it “switched off.” Simultaneously, our lncRNA recruits proteins to the strand to place epigenetic markers such as methyl or acetyl tags on the DNA bases or histones on the chromatin. These tags alter the expression of that stretch of DNA without actually changing the sequence.
Some epigenetic changes, though, do alter the DNA sequence. They can mark a cytosine (C) base for replacement with a thymine (T). Scientists have noticed this often occurs at C’s followed by guanine (G). This means that the next generation after a cell division can actually inherit an altered code.

Although these ideas have yet to be substantiated by complete experimental evidence, one can envision this as a model for how the system might work — a mechanism by which epigenetic changes, guided by lncRNAs, could make permanent and heritable changes to the genome. Indeed, such a lncRNA-based DNA editing system could be driving some aspects of genetic variation and could explain the common appearance of single nucleotide polymorphisms within a species.

These epigenetic changes might function to provide variability to the offspring to enable it to survive a changing environment. They might cause that stretch of DNA to increase or decrease its expression. If the section of code is for a lncRNA, it might produce a transcript that folds differently, turning off its ability to bind to a target transcript the next time, allowing the “silenced” gene to be expressed. The lncRNA might, therefore, have a built-in mechanism for regulating itself.

One can begin to envision how environmental variation, by instigating epigenetic changes, could increase organismal complexity, thus giving populations a greater chance at surviving new and perhaps permanent environmental threats. In other words, epigenetics, rather than random genetic point mutations, could provide the missing link between environmental pressure and the resulting genetic variability that generates robustness of a species.

It is “not out of the realm of possibility” that such processes work in humans. Morris cites a 2008 study on offspring of the Dutch famine of 1944-1945. Children born during the famine had distinct epigenetic markers their siblings born before or after it did not. The markers affected insulin production, and thereby growth. They lasted for several decades. Although these environment-driven changes might have occurred in utero instead of in the DNA, the study raised the possibility that epigenetics is a designed mechanism to help organisms cope with stressful situations, then rebound when the stresses are relieved.
None of these cutting-edge discoveries sounds like classical Darwinism. Morris realizes this and gives a slight bow to Lamarck, while marveling at the complexity that neither Lamarck or Darwin could have realized:

The inner molecular workings of the cell are vastly complex, and the emerging realization that lncRNAs are active modulators of gene transcription and epigenetic states only complicates the picture. Clearly, as more data emerges in this exciting area of research, additional layers of regulation will need to be added to the central dogma of molecular biology. Although an organism cannot pass down specific information about its own experiences — the giraffe will not be able to help its offspring reach taller trees just by stretching its own neck — it may give succeeding generations a fighting chance in a difficult environment by offering them a slightly altered arsenal of genetic tools.

We remind readers, at this point, that the death of “junk DNA” and the existence of “additional layers of regulation” were predictions of intelligent design, not of neo-Darwinism.
Image: ralph and jenny/Flickr.