Figure 1.

Loss of kismet Provokes ISC Accumulation without Affecting Terminal Differentiation

(A) The ISCs divide to self-renew and to produce a precursor cell, the EB, that subsequently terminally differentiates into an EC or is thought to divide once as an EEP to produce two EE cells.

(B and C) Wild-type (B) and kis^10D26 mutant (C) MARCM clones, 5 days after heat shock (AHS).

(D) Quantification of (B) and (C).

(E) Scheme of wild-type and kismet mutant clones.

(F) Scheme of kismet gene and Kismet protein (Long and short isoforms: Kis L and Kis S): chromodomains (green), ATPase domain (red), BRK domain (blue). All kis alleles resulted in nonsense mutations: nucleotide changes and corresponding putative resulting truncated proteins are shown.

(G–L) Wild-type and kis^10D26 MARCM clones at 9 days AHS. Arrows in (G)–(H′) and (I)–(J′) show EE cells marked by DH31 or LTK2, respectively.

(M–P) Quantification of the total cells per clone (M), number of EE cells per clone (Prospero+) (N), number of ECs (Pdm1+ cells per clone) (O), and the ratio of EE (Prospero+ cells / EC (polyploid nucleus >7 μm) per clone (P).

(Q and R) Vertical sections through the midgut epithelium of control (Q) and kis^10D26 mutant (R) MARCM clones, 9 days AHS. Arrows show apical membrane.

In (D) and (M)–(P), A two-tailed Mann-Whitney statistical test was used; mean values in red; error bars, SEM; ns = non-significant, **p < 0.01, ****p < 0.0001. Scale bars, 20 μm.