Transit-Amplifying Cells in the Fast Lane from Stem Cells towards Differentiation

Table 2

Genes expressed in SCs	Genes expressed in TACs	Organ or tissue	Putative TAC function	References
GFRα1+	GFRα1−/Miwi2+/Ngn3+	Testis	Represent a novel subpopulation of undifferentiated spermatogonium. Also involved in TAC pluripotency	[24]
β1 integrins^Hi/α6 integrin^Hi/CD71^Low/delta1^Hi/desmoglein 3^Low/EGFR1^Low/Lrig1^Hi MCSP+/delta1+	β1 integrins^Low MCSP−/delta1−	Epidermal cells	May represent a new population without any characterized function	[88–90]
Reg4	Reg4/ribosomal genes	Intestinal epithelium	TAC populations migrating upward along the intestinal crypt-villus axis	[87]
β1 integrin^Hi/keratin14 p63 ^Hi/Pp63^Low	β1 integrin^Low/p63 ^Low/Pp63^Hi	Clonogenic cultures and keratinocytes cultures	Increased p63 phosphorylation marks the exit from SC state and could be used to detect epidermal cell stratification	[16, 18]
Gas1+ in Bu-SCs/SHH−	Gas1−/SHH+	Hair follicle in mammals	TACs act as a signaling center between Bu-SCs and DP promoting their proliferation. TACs integrate the timing and frequency for two populations of SCs	[59]
p63/PCNA in basal cells	p63/PCNA in suprabasal cells	Zebrafish epidermis	A proliferation shift from basal to suprabasal cells marks the stratification process	[46]
Jak-STAT signaling		Drosophila spermatogonium	The ability of TACs to respond to signals from the SC niche and dedifferentiate into SCs	[22]
Symmetric cell division (SCD); MINSC-PAR3- and LGN- uncoupling of NuMA	Asymmetric cell division (ACD); MINSC^Hi, PAR3^Hi, LGN^Hi in complex with NuMA	Epidermis stratification	Asymmetric division is essential for TACs formation	[33–39]
p21^Hi/p27^Hi/RB dephosphorylated (active form)	CDK2^Hi CDK4^Hi/p21^Low/RB phosphorylated^Down (inactive form)	Mouse pituitary gland and hematopoietic cells	Events that may trigger TAC cell proliferation	[49–51]