Background: Epidermal homeostasis involves the monitoring of continuous proliferative and differentiative processes as keratinocytes migrate from the basal layer to the skin surface. Recently, differentiation of epidermal stem cells was shown to be promoted by the Notch pathway. This pathway is characterised by cell-cell interactions between transmembrane proteins and was first implicated in lateral inhibition, patterning and cell binary choices during embryogenesis.

Nucleotide sequence reagents are verifiable experimental reagents in biomedical publications, because their sequence identities can be independently verified and compared with associated text descriptors. We have previously reported that incorrectly identified nucleotide sequence reagents are characteristic of highly similar human gene knockdown studies, some of which have been retracted from the literature on account of possible research fraud. Because of the throughput limitations of manual verification of nucleotide sequences, we developed a semi-automated fact checking tool, Seek & Blastn, to verify the targeting or non-targeting status of published nucleotide sequence reagents. From previously described and unknown corpora of 48 and 155 publications, respectively, Seek & Blastn correctly extracted 304/342 (88.9%) and 1066/1522 (70.0%) nucleotide sequences and a predicted targeting/ non-targeting status. Seek & Blastn correctly predicted the targeting/ non-targeting status of 293/304 (96.4%) and 988/1066 (92.7%) of the correctly extracted nucleotide sequences. A total of 38/39 (97.4%) or 31/79 (39.2%) Seek & Blastn predictions of incorrect nucleotide sequence reagent use were correct in the two literature corpora. Combined Seek & Blastn and manual analyses identified a list of 91 misidentified nucleotide sequence reagents, which could be built upon through future studies. In summary, incorrect nucleotide sequence reagents represent an under-recognized source of error within the biomedical literature, and fact checking tools such as Seek & Blastn may help to identify papers and manuscripts affected by these errors.

The structure of the four murine Hox complexes and the co-ordinate expression patterns of Hox genes have been elucidated for almost a decade. However, clues about their developmental functions have been recently uncovered from the analysis of loss-of-function mutants generated by the gene targeting technique, as well as from transgenic mice with altered Hox gene expression domains. The 'anterior' Hox genes control the morphogenetic programme of specific hindbrain segments (rhombomeres) or pharyngeal arch neural crest derivatives. Various studies indicate that Hox gene products act in a region-specific, combinatorial and partly redundant manner to specify the identities of developing vertebrae. In addition, 'posterior' HoxA and HoxD genes act coordinately to control the growth and morphogenesis of skeletal structures along the proximodistal axis of developing limbs. Studies in other vertebrate model systems suggest that the evolution of Hox gene functions has allowed for the acquisition of specific morphological features along both the vertebral column and limbs of tetrapods. Gene targeting studies have also revealed region-specific functions of Hox genes along the developing digestive and genito-urinary tracts.