My very own copy of Molecular Endocrinology

The February issue of Molecular Endocrinology is hanging out with all of our regular magazines for awhile.

Why, you might ask?

Because Jonathon is published in it!

I know that someday we won't be so excited about every publication, but for now... we discuss the research for months beforehand, anxiously await news of its acceptance into a journal, and then lovingly take pictures and blog about it. Such is the life of a PhD student (and family). Each publication is an important step in a long journey and represents a lot of hard work.

2 down, 2 to go. Great Job, Jonathon!

Oh, and if you are interested in a taste of what the article is about, I have included the abstract. Just to warn you... I have no idea what it is saying.

Nkx2.2 is an essential regulator of pancreatic endocrine differentiation. Nkx2.2 null mice are completely devoid of beta cells and have a large reduction of alpha and PP cells. In the place of these islet populations, there is a corresponding increase in the ghrelin-positive epsilon cells. Molecular studies have indicated that Nkx2.2 functions as an activator and repressor to regulate islet cell fate decisions. To determine whether Nkx2.2 is solely important for islet cell fate decisions or also has the capability to control ghrelin at the promoter level, we studied the transcriptional regulation of the ghrelin promoter within the pancreas, in vitro and in vivo. These studies demonstrate that both of the previously identified transcriptional start sites in the ghrelin promoter are active within the embryonic pancreas; however, the long transcript is preferentially upregulated in the Nkx2.2 null pancreas. We also show that the promoter region between -619 and -488 base pairs upstream of the translational start site is necessary for repression of ghrelin in alphaTC1 and betaTC6 cells. Surprisingly, we also show that Nkx2.2 is able to bind to and activate the ghrelin promoter in several cell lines that do or do not express endogenous ghrelin. Together these results suggest that the upregulation of ghrelin expression in the Nkx2.2 null mice is not due to loss of repression of the ghrelin promoter in the non-ghrelin islet populations. Furthermore, Nkx2.2 may contribute to the activation of ghrelin in mature islet epsilon cells.