In contrast to what has been reported in mice, we observed elevated embryonic lethality in brc-1 and brd-1 null alleles [brc-1(xoe4), brd-1(xoe18) (Li et al. 2023; Li et al. 2018)], in combination with either hsr-9(ok759) (Ryu et al. 2013) or a new putative null allele hsr-9(xoe17) (Figure 1A).
In contrast to what has been reported in mice, we observed elevated embryonic lethality in brc-1 and brd-1 null alleles [brc-1(xoe4), brd-1(xoe18) (Li et al. 2023; Li et al. 2018)], in combination with either hsr-9(ok759) (Ryu et al. 2013) or a new putative null allele hsr-9(xoe17) (Figure 1A).
In contrast to what has been reported in mice, we observed elevated embryonic lethality in brc-1 and brd-1 null alleles [brc-1(xoe4), brd-1(xoe18) (Li et al. 2023; Li et al. 2018)], in combination with either hsr-9(ok759) (Ryu et al. 2013) or a new putative null allele hsr-9(xoe17) (Figure 1A).
In contrast to what has been reported in mice, we observed elevated embryonic lethality in brc-1 and brd-1 null alleles [brc-1(xoe4), brd-1(xoe18) (Li et al. 2023; Li et al. 2018)], in combination with either hsr-9(ok759) (Ryu et al. 2013) or a new putative null allele hsr-9(xoe17) (Figure 1A).
On the other hand, a hypomorphic brc-1 allele, brc-1(tm1145) (Li et al. 2018), in combination with hsr-9(xoe17) did not result in elevated embryonic lethality (Figure 1A).
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.