Table 1 Notch signaling mouse mutants with MuSC phenotype

 Rbpj

Tg:Pax7-CreERT2; Rbpj^flox/-

Spontaneous differentiation, bypassing S-phase. Reduction of quiescent pool starting at 16 days post-tamoxifen induction. Failure to self-renew.

[18]

 Rbpj

Pax7^CreER; Rbpj^flox/flox

idem

[14]

 Rbpj

Lbx1^Cre; Rbpj ^flox/flox

Precocious differentiation, muscle hypotrophy.

[20]

 Rbpj; Myod dKO

Pax3^Cre/+; Rbpj^flox/+; Myod^−/−

Rescued differentiation,

disrupted homing under the basal lamina.

[26]

 Notch1

Pax7^CreERT2/+; Notch1^{flox/ flox} (post-natal day P7 induction)

Failure to enter quiescence at 4 weeks of age, differentiation, and eventual reduction of pool size.

[27]

 Notch1

Pax7^CreERT2/+; Notch1^{flox/ flox} (adult induction, 7-14w old)

No phenotype up to 19 days post-tamoxifen induction.

[28]

 Notch2

Pax7^CreERT2/+; Notch2 ^flox/flox (adult induction, 7-14w old)

Reduction of pool at 5 days post-tamoxifen induction.

[28]

 Notch1/Notch2

Pax7^CreERT2/+; Notch1^flox/flox; Notch2 ^flox/flox (adult induction, 7-14w old)

Drastic reduction of pool 5 days post-tamoxifen induction.

[28]

 Notch3

Germline Notch3−/−

Increased size of quiescent pool, increased proliferation in culture. Muscle hyperplasia following repetitive muscle injuries.

[29]

 N1-ICD O/E

Pax7^CreERT2/+; R26^NICD-nGFP (post-natal day P7 induction)

Enter premature quiescence 3 days post-tamoxifen induction

[27]

 N1-ICD O/E

Myf5^Cre/+; R26^NICD-nGFP

Inhibition of differentiation and sustained proliferation at embryonic stages. Enter premature quiescence at fetal stages. Muscle hypotrophy.

[23]

 N1-ICD O/E

Pax7^CreER; R26^{NICD-nGFP x}

Upregulation of Pax7 independently of Myod inhibition. Inhibition of quiescence exit following isolation.

[30]

 Dll1

Dll1^hypomorphic/Dll^null

Precocious differentiation, muscle hypotrophy.

[19]

 Dll1

Pax7^CreERT2; Dll1^flox//flox

No impact on quiescence or activation. Premature differentiation, impaired self-renewal, and myofiber diameter severely reduced upon regeneration.

[31]

 Dll4

HSA^CreMER; Dll4 ^flox/flox

Reduction of quiescent pool.

[32]

 Dll4

Pax7^CreERT2; Dll4 ^flox/flox

No impact on quiescence.

[32]

 Hey1/HeyL co-dKO

Pax7^CreERT2/+; Hey1^flox/flox; HeyL^–/–

Pool size reduced 3 weeks post-tamoxifen injection. Reduced weight of regenerated muscle and increased fibrosis.

[33]

 Hes1

Pax3^Cre/+; Hes1^flox/flox

Reduced pool size at post-natal day 28. Subtle effect on the overall muscle size at birth, severely affected muscle growth during post-natal development.

[34]

 Hes1/HeyL

Pax3^Cre/+; Hes1^flox/flox; HeyL−/−

Greater reduction of pool size compared to single coHes1.

[34]

 Col5a1

Tg:Pax7-CreERT2; Col5a1^flox/flox

Spontaneous differentiation, reduction of quiescent pool starting at 3 weeks post-tamoxifen induction. Failure to self-renew.

[35]

 mircroRNA-708

WT (injected antagomir)

Spontaneous migration and differentiation by targeting Tensin3 transcripts.

[36]

 Pten

Pax7^CreERT2/+; Pten ^flox/flox

Spontaneous activation of quiescent MuSCs and premature differentiation without proliferation (reach S-phase but seem not to complete the cell cycle). Failure to self-renew.

[37]

 Mettl3

Pax7^CreERT2; Mettl3^flox/flox

No impact on quiescence. Inhibition of proliferation, impaired regeneration.

[38]

 Adam10

Pax7^CreERT2/+; Adam10 ^flox/flox

Reduction of quiescent pool, regeneration defect.

[39]

 Foxo3

Pax7^CreER; Foxo3 ^flox/flox

Impaired self-renewal and increased propensity to differentiate.

[40]