Figure 4. Increased adhesion is not causal to niche competition.

A, B ptc mutant clones did not upregulate adhesion molecules. No change in βPS-integrin (A, red, single channel in A’) or in DE-cadherin expression (B, blue, single channel in B’) was seen at the hub in testes with ptc mutant clones (green). Vasa labels germ cells in red (B), Tj labels somatic cells in blue (A). The hub is indicated with a dotted line.

C, D GFP-positive MARCM clones (green, single channels in C’,D’) overexpressing βPS-integrin (C) or DE-cadherin (D) did not outcompete neighboring wild-type CySCs or GSCs. Vasa labels germ cells in red, Tj labels somatic cells in blue. The hub is indicated with a dotted line.

E, F Control (E) and rhea mutant (F) MARCM clones showing marked CySCs which contacted the hub at 7 dpci (arrows). Vasa labels germ cells in red, Tj labels somatic cells in blue. The hub is indicated with a dotted line.

G CySC clone recovery rates at 2 (blue bars) and 7 (red bars) dpci for control (left) and rhea mutant (right). The presence of rhea mutant clones at the niche at the 7-day time point indicates that rhea was not required in CySCs for self-renewal. n = 38 and 24 for control at 2 and 7 dpci, respectively, and n = 9 and 49 for rhea¹ at 2 and 7 dpci, respectively.

H Number of GSCs present when CySC clones of the indicated genotype were generated at 14 dpci. Overexpression of βPS-integrin, TalinH or DE-cadherin did not affect GSC numbers. n = 15, 19, 25, 17 for control, UAS-βPS-integrin, UAS-TalinH or UAS-DE-cadherin, respectively. Error bars denote SEM.

I Number of GSCs when ptc mutant CySC clones were present along with a single mutant copy of the indicated genes at 14 dpci. Reduction of α-cat had no effect on the ptc phenotype, while one rhea allele partly suppressed GSC loss. n = 48 (control); 21 (control; rhea¹/+); 49 (ptc); 26 (ptc; α-cat/+); 19 (ptc; rhea^6-66/+); 35 (ptc; rhea¹/+). Error bars denote SEM.