Differential regional expression of multiple ADAMs during feather bud formation

Abstract

The expression of seven members of the ADAM family was investigated by in situ hybridization in the developing feather buds of chicken. The expression profiles of the ADAMs in the cells and tissues of the feather buds differ from each other. ADAM9, ADAM10, and ADAM17 are expressed in the epidermis of the feather bud, whereas ADAM23 expression is restricted to the bud crest, with a distribution similar to that of sonic hedgehog. ADAM13 is not only expressed in the epidermis, but also in restricted regions of the dermis. Both ADAM12 and ADAM22 are expressed in the dermis of the feather bud, with an opposite mediolateral and anteroposterior polarity. Furthermore, the mRNAs of all investigated ADAMs show regional differences in their expression, for example, in the neck and in the roots of the leg and wing. These results suggest that ADAMs play a variety of roles during avian feather bud formation. Developmental Dynamics 240:2142-2152,

Identification of Secreted Exoproteome Fingerprints of Highly-Virulent and Non-Virulent Staphylococcus aureus Strains

“…It is known, however, that HLA uses ADAM 10 as a receptor and HLA-driven toxicity depends on the amount of this receptor which differs among cell types and/or the source species (Berube and Bubeck Wardenburg, 2013 ). High expression of ADAM 10 documented in many tissues of the chicken embryo (Hall and Erickson, 2003 ), including epidermis during formation of feather buds (Lin et al, 2011 ) indirectly suggests possible involvement of HLA in staphylococcal virulence in this specie, however direct evidence is missing. Secretion of HLA in in vitro cultures characterizes particular clonal types of S. aureus , among other, lineage CC5 (Monecke et al, 2014 ).…”

Development, Regeneration, and Evolution of Feathers

“…Broad-spectrum MMP inhibitors and TIMP2 each suppressed feather bud development (44). In a separate study, the distribution of ADAMs (adisintegrin and metalloproteases), which bind to integrins and possess metalloprotease activity, was determined (45). In the dorsal tract, ADAM9, 10, 17, and 23 were expressed in the feather bud epidermis, whereas ADAM12 and 22 were expressed in the dermis.…”

Coordinating Gene Expression and Axon Assembly to Control Axon Growth: Potential Role of GSK3 Signaling

“…Many of these proteins are well-established GSK3 substrates, including CREB, NFATc, p53, NFκB, c-Jun, and Smads (see discussion below). Although some have not been identified directly as GSK3 substrates, including SRF, Sox11, Id2, and KLFs (Lasorella et al, 2006; Wickramasinghe et al, 2008; Moore et al, 2009; Jing et al, 2011; Lin et al, 2011; Yu et al, 2011), they contain multiple and well-conserved GSK3 sites (Taelman et al, 2010). In this section, we summarize the functions of these proteins in regulation of axon growth and discuss how they are regulated by the GSK3 signaling.…”

“…During development, several transcription factors have been shown to control axon growth downstream of neurotrophin signaling, including CREB (Lonze et al, 2002), NFATc (Graef et al, 2003), SRF (Wickramasinghe et al, 2008), and Sox11 (Lin et al, 2011), among which CREB and NFATc are well-established GSK3 substrates. Upon neurotrophin stimulation, CREB is activated via Serine-133 phosphorylation downstream of the MAPK pathway (Bonni et al, 1995; Finkbeiner et al, 1997; Arthur et al, 2004).…”