The latest issue of the journal Science (Aug. 1, 2016) has an article on a recent paper by Aires et al. (2016) published in Developmental Cell. Here's the abstract of the paper ...
Vertebrates exhibit a remarkably broad variation in trunk and tail lengths. However, the evolutionary and developmental origins of this diversity remain largely unknown. Posterior Hox genes were proposed to be major players in trunk length diversification in vertebrates, but functional studies have so far failed to support this view. Here we identify the pluripotency factor Oct4 as a key regulator of trunk length in vertebrate embryos. Maintaining high Oct4 levels in axial progenitors throughout development was sufficient to extend trunk length in mouse embryos. Oct4 also shifted posterior Hox gene-expression boundaries in the extended trunks, thus providing a link between activation of these genes and the transition to tail development. Furthermore, we show that the exceptionally long trunks of snakes are likely to result from heterochronic changes in Oct4 activity during body axis extension, which may have derived from differential genomic rearrangements at the Oct4 locus during vertebrate evolution.... those ignorant of history are not condemned to repeat it; they are merely destined to be confused.
Stephen Jay Gould
Ontogeny and Phylogeny (1977)The results were written up by a freelance journalist named Diana Crow [‘Junk DNA’ tells mice—and snakes—how to grow a backbone]. She writes ...
‘Junk DNA’ tells mice—and snakes—how to grow a backboneSandwalk readers will see all the mistakes and misconceptions in these paragraphs. She's talking about regulatory sequences that were never, ever, thought to be junk. The paper being discussed has nothing to do with junk DNA and the results do not in any way alter our understanding of developmental gene regulation.
Why does a snake have 25 or more rows of ribs, whereas a mouse has only 13? The answer, according to a new study, may lie in "junk DNA," large chunks of an animal’s genome that were once thought to be useless. The findings could help explain how dramatic changes in body shape have occurred over evolutionary history.
Scientists began discovering junk DNA sequences in the 1960s. These stretches of the genome—also known as noncoding DNA—contain the same genetic alphabet found in genes, but they don’t code for the proteins that make us who we are. As a result, many researchers long believed this mysterious genetic material was simply DNA debris accumulated over the course of evolution. But over the past couple decades, geneticists have discovered that this so-called junk is anything but. It has important functions, such as switching genes on and off and setting the timing for changes in gene activity.
I wish to emphasize one other distinction. Evolution occurs when ontogeny is altered in one of two ways: when new characters are introduced at any stage of development with varying effects upon subsequent stages, or when characters already present undergo changes in developmental timing. Together, these two processes exhaust the formal concept of phyletic change.; the second process is heterochrony. [my emphasis ... LAM] If change in developmental timing is important in evolution, then this second process must be very common.This was written in 1977—that's almost 40 years ago! These ideas were around for decades before Gould wrote his book1 and they have been shown to be correct by numerous studies in the 1980s.
What's going on here? Science is supposed to be one of the leading science journals. How could it publish an article that misrepresents the field so badly? Do the editors send these "Latest News" articles out for review?
1. Ed Lewis shared the Nobel Prize in 1995 for his contribution to "the genetic control of early embryonic development" [The Nobel Prize in Physiology or Medicine 1995].