"RNAi inhibition of CBP-1 induces ectopic expression of HLH-2::GFP in non-neuronal cells (Figure 4B, compare panels a and b; Shi and Mello, 1998), a promoter who's activity is restricted to neurons late in C. elegans embryogenesis (Krause et al., 1997). In contrast, inhibition of CBP-1 by RNAi eliminated the expression of HLH-1::GFP and ELT-2::GFP (Figure 4B, compare panels e and h with d and g), promoters that are active in muscle and endodermal cells, respectively (Krause et al., 1990; Fukushige et al., 1998)."
"RNAi inhibition of CBP-1 induces ectopic expression of HLH-2::GFP in non-neuronal cells (Figure 4B, compare panels a and b; Shi and Mello, 1998), a promoter who's activity is restricted to neurons late in C. elegans embryogenesis (Krause et al., 1997). In contrast, inhibition of CBP-1 by RNAi eliminated the expression of HLH-1::GFP and ELT-2::GFP (Figure 4B, compare panels e and h with d and g), promoters that are active in muscle and endodermal cells, respectively (Krause et al., 1990; Fukushige et al., 1998)."
"RNAi inhibition of CBP-1 induces ectopic expression of HLH-2::GFP in non-neuronal cells (Figure 4B, compare panels a and b; Shi and Mello, 1998), a promoter who's activity is restricted to neurons late in C. elegans embryogenesis (Krause et al., 1997). In contrast, inhibition of CBP-1 by RNAi eliminated the expression of HLH-1::GFP and ELT-2::GFP (Figure 4B, compare panels e and h with d and g), promoters that are active in muscle and endodermal cells, respectively (Krause et al., 1990; Fukushige et al., 1998)."
In a strong gld-2 loss-of-function allele(q497) CGH-1 was appropriately upregulated at meiosis entr y and appeared to be localized normally through the pachytene stage, but expression of both CGH-1 and PGL-1 was lost more proximally, in the abnormal gametes that are produced.
In a strong gld-2 loss-of-function allele(q497) CGH-1 was appropriately upregulated at meiosis entr y and appeared to be localized normally through the pachytene stage, but expression of both CGH-1 and PGL-1 was lost more proximally, in the abnormal gametes that are produced.
In a strong gld-2 loss-of-function allele(q497) CGH-1 was appropriately upregulated at meiosis entr y and appeared to be localized normally through the pachytene stage, but expression of both CGH-1 and PGL-1 was lost more proximally, in the abnormal gametes that are produced.
In a strong gld-2 loss-of-function allele(q497) CGH-1 was appropriately upregulated at meiosis entr y and appeared to be localized normally through the pachytene stage, but expression of both CGH-1 and PGL-1 was lost more proximally, in the abnormal gametes that are produced.
In a strong gld-2 loss-of-function allele(q497) CGH-1 was appropriately upregulated at meiosis entr y and appeared to be localized normally through the pachytene stage, but expression of both CGH-1 and PGL-1 was lost more proximally, in the abnormal gametes that are produced.