This post is by M.Mar Albà on her preprint (with co-authors) available from arRxiv Long non-coding RNAs as a source of new peptides.

Several recent studies based on deep sequencing of ribosome protected fragments have reported that many long non-coding RNAs (lncRNAs) associate with ribosomes (see for example Everything old is new again: (linc)RNAs make proteins! a comment by Stephen M Cohen). We have analyzed the original data from experiments performed in six different eukaryotic species and confirmed that this is a widespread phenomenon. This is paradoxical because lncRNAs apparently have very little coding capacity with only short open reading frames (ORFs) that do not show sequence similarity to known proteins.

In contrast to typical mRNAs, many lncRNAs are lineage-specific. Therefore, if they are translated, they should be similar to recently evolved protein-coding genes. This is exactly what we have found. It turns out that transcripts encoding young proteins show very similar properties to lncRNAs; short and non-conserved ORFs, low coding sequence potential, and relatively weak selective constraints.

Evidence has accumulated in recent years that new protein-coding genes are continuously evolving (The continuing evolution of genes by Carl Zimmer). The birth of a new functional protein is a process of trial and error that most likely requires the expression of many transcripts that will not survive the test of time. LncRNAs seem to fit the bill for this role.

This guest post is by Paul Bilinski on his paper with coauthors Diversity and evolution of centromere repeats in the maize genome BioRxived here.

Centromeres have the potential to play a central role in speciation, yet our ability to study them has been limited because of their repetitive nature. The centromeres of many eukaryotes consist partly of large arrays of short tandem repeats, though the actual sequence of the repeat varies widely across taxa. To investigate the whether the variation found in the tandem repeats themselves could inform our understanding of their evolutionary history we made use of the reference maize genome as well as resequencing data from several lines of maize and its wild relative teosinte.

Although tandem repeats should be identical upon duplication, our analysis of CentC in maize revealed that most copies genome-wide are unique. We observed only three instances where adjacent copies were identical in sequence and length, driving home the idea that these tandem repeats have accumulated immense diversity. Given such diversity, we wanted to investigate genetic relatedness across CentC copies.

Using positional and genetic relatedness information from the fully-sequenced centromeres 2 and 5, we found high within-cluster similarity, suggesting that tandem duplications drove most CentC copy number increase. Contrary to patterns seen in Arabidopsis (Kawabe and Nasuda 2005), principle coordinate analysis of repeats found no clustering by chromosome, with groups of CentC with similar sequence distributed across all of the chromosomes.

Another surprising discovery involved the origin of the biggest arrays of CentC. As an ancient tetraploid maize originally had 20 chromosomes with 20 centromeres. Processes of fractionation and rearrangement have led to the 10 chromosomes in the extant maize genome. Schnable et al (2011) were able to identify which chromosomal segments derive from each of maize’s ancient parents, referred to as subgenomes one and two. Wang and Bennetzen (2011) built on this information, and found that about half of the modern centromeres came from each parent. Inferring subgenome of origin by flanking regions, we found that all of the CentC clusters >20kb in length derive from subgenome 1. The proportions are less skewed when looking at clusters >10kb, though in all cases we see more bp of CentC assigned to subgenome 1 than we expect based on its total bp in the genome. This is particularly interesting because subgenome 1 also shows higher overall gene expression and fewer deletions than subgenome two (Schnable et al 2011).

The diversity of CentC seen might suggest that CentC repeats were reasonably static in the genome, persisting in the same spot for a long time with occasional increases in copy number via tandem duplication. However, fluorescent in situ hybridization suggested that domestication resulted in a large loss of CentC signal across many of maize’s 10 chromosomes. We confirmed and quantified the loss of CentC using resequencing data from a set of maize and teosinte lines (Chia et al. 2012).

Combined, our results suggest long term stability of CentC clusters with new copies arising from tandem duplication, while mutation serves to homogenize rather than separate clusters. We hope our insights into centromere repeat evolution will build toward a better understanding of their role in evolution.

This guest post is by Justin Blumenstiel on his preprint (with co-authors) When genomes collide: multiple modes of germline misregulation in a dysgenic syndrome of Drosophila virilis, available from bioRxiv here.

Does the activation of one transposable element (TE) family typically lead to the activation of many? If so, this would indicate a synergism between different TE families with significance for TE dynamics in natural populations. A standard model of TE dynamics typically takes into account population size, transposition rate (which may vary based on host defense) and selection against TE insertions. If the mobilization of one TE can lead to the mobilization of others, the transposition rate of one TE family could influence the transposition rate of others.

Hybrid dysgenic syndromes in Drosophila are an important model for TE dynamics when one TE family becomes mobilized. In the 1980’s, it was generally concluded that P element dysgenesis did not lead to mobilization of other TEs. However, studies in the D. virilis system of hybrid dysgenesis indicated otherwise. More recently, an analysis of transposition in the P element system indicated movement of elements other than the P element. Thus, it appears that co-mobilization may be a common feature of dysgenic syndromes.

What is the mechanism of co-mobilization? For the P element system, studies by William Theurkauf and colleagues point to the DNA damage response as key. Specifically, via Chk2 kinase, DNA damage signaling leads to perturbed piRNA biogenesis, which in turn leads to the activation of other elements under control of piRNA-based silencing. Does this mechanism also apply to other systems?

To study the mechanism of TE co-mobilization in the D. virilis system, we performed small RNA sequencing and mRNA sequencing experiments using germline material of reciprocal females of the dysgenic and non-dysgenic crosses. In contrast to the P element and I element systems, hybrid dysgenesis in D. virilis is more complex. For one, there is not a single element that has been proven to be the sole cause. This was previously shown, but in this study we identified several more elements that likely contribute. From small RNA sequencing, we find that TE mis-expression persists in the progeny of the dysgenic cross, without a persisting global defect in piRNA biogenesis. Rather, it appears that piRNA biogenesis defects are idiosyncratic across different TE families. Interestingly, we also find evidence that piRNA silencing loses specificity in the dysgenic cross, with some highly expressed genes becoming non-specific targets.

Overall, this study provided several insights, but the mechanism of co-mobilization in the D. virilis system remains unknown. The complexity of this syndrome makes it a challenge for study, but it may provide significant insight into genome dynamics of hybrids whose parents differ for more than one TE family. Future genetic analysis may allow us to determine the role of the DNA damage response in maintaining the activity of some TE families, but not others.