It is easy to understand the difference between the whole body knockout between tissue specific knockout. But I am wondering about the difference between pancreas-, islet-, β-cell-specific knockout. What's more, which is more welcome in nowadays research work, especially related to diabetes and insulin?
It depends on the question you want to answer, I suppose. To begin with, I am not sure that "pancreas-specific" knockout is very helpful, given that the majority of pancreas is involved in exocrine secretion. I would be surprised to find that there were promoters which led specifically to expression in the entire pancreas (both exocrine and endocrine). I may be wrong, and if so, then I'm sure someone will correct me. When, in the diabetes world, people refer to pancreas specific knockout, I think they tend to mean endocrine-pancreas specific, and so this term is synonymous with islet knockout.
In terms of islet vs beta-cell specific knockouts, then the difference is more interesting. There is a lot of paracrine cross talk within the islet, and so differentiating between primary effects (i.e. mediated directly by action on the cell-type of interest) from secondary effects (i.e. mediated by paracrine effects on the cell of interest following primary effects on a different cell-type) may well be very interesting and yield important understanding. Here, a platform of cell-type specific knockouts might be interesting.
I don't know of any promoters which can be used to specifically drive knockout in all types of cells in the pancreatic iselts (again, someone else may be able to correct this), but Ins1, Ins2 and Pdx promoters have all been used to drive fairly specific beta-cell knockout (there is some ectopic Cre expression in the brain)
Thanks David! You gave the answers exactly I am looking for and your analysis turns out to be excellent! I hardly have an idea of Cre and its work mechanism. But it doesn't matter, this interesting question may push me to search for more information. Thank you for your kindness!
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