Fate plasticity in the intestine: The devil is in the detail

Table 1 Mouse injury models used for plasticity studies

Study	Plastic cell identified	Injury model used
Tian et al[18]	Bmi1+ cell	DTR Lgr5+ ablation
Roth et al[19]	Paneth cell	12Gy radiation
van Es et al[16]	Dll1+ cell	6Gy radiation
Buczacki et al[17]	Label-retaining cell	6Gy radiation, doxorubicin or hydroxyurea
Asfaha et al[20]	Upper crypt progenitor	12Gy radiation +/- 5-Fluorouracil
Tetteh et al[27]	Alpi1+ enterocyte	DTR Lgr5+ ablation
Jadhav et al[9]	Goblet cell progenitors	DTR Lgr5+ ablation
Yan et al[21]	Enteroendocrine cell	12Gy radiation
Ishibashi et al[22]	Atoh1+ cell	DSS (1.75%) for 5 d
Nusse et al[23]	Lgr5- crypt cell	Parasite infection
Schmitt et al[24]	Paneth cell	DSS (3%) for 1 wk
Tomic et al[26]	Atoh1+ cell	6Gy radiation, AOM or 2% DSS
Yu et al[25]	Lyz1+ Paneth cell	12Gy radiation
Castillo et al[28]	Atoh1+ cell	DSS (2.5%-3%) for 5 d

Table 2 Concepts leading to difficulties in ascribing behaviour to cell types in the intestine

CreER and Tamoxifen	Toxicity
	Off-target effects
Incongruity between reporter expression and protein expression	Regional differences
	Chronicity of reporter stability
	Reporter and mRNA expression differences
Inconsistent injury models	Intestinal specific effects including incomplete cell type eradication e.g., diphtheria toxin mediated cell death
	Off-target whole body effects e.g., irradiation
	Representative of “homeostatic regeneration”
	Different cell-type responses to different injuries
Laboratory differences	Microbiota
	Diet
	Area of intestine examined
	Strain differences between laboratories due to inbreeding