@McKnightLab_UO was an inspiring champion of students overcoming challenges. Please join us in further imprinting Jeff's legacy.

10/ Shh is the zone of polarizing activity (ZPA) morphogen that patterns developing limbs, including digits that may share deep homology with rays. Here, we show ray branching is the same in all paired and unpaired fins.

6/ These movements slow in a Shh/Smo-dependent manner when bEps are tightly juxtaposed with pObs and upregulate shha. bEps then accelerate as they pass beyond pObs and downregulate shha.

5/ We use live imaging to show the basal epidermal cells that comprise each shha-expressing domain are rapidly and constantly turned over by their collective distal migration.

4/ We find Shh/Smo is largely dedicated to ray branching, with surprisingly little effect on earlier appendicular skeletal patterning or outgrowth.

3/ We use transgenic reporters and Kaede photoconversion to show constant Shh/Smo activity in narrow bands of shha-expressing basal epidermal cells (bEps) and immediately adjacent progenitor osteoblasts (pObs).

2/ As during regeneration, patches of shha-expressing basal epidermal cells in the distal aspect of juvenile fins split in advance of ray branching.

Huge congrats on the well-deserved award! Follow @ZfishAmy to learn how fin rays provide a gorgeous model of branching morphogenesis.

7/ Blastula transplantations and F0 CRISPRants show longfin-originating Kcnh2a acts fin autonomously and within the intra-ray mesenchyme lineage that generates the niche pool. Concordantly, kcnh2a is ectopically expressed in intra-ray mesenchyme and niche cells of longfin fins.

4/ A kcnh2a CRISPR-generated mutant perfectly rescues longfin fin overgrowth back to wildtype extents. Kcnh2a is therefore the long mysterious cause of longfin (t2!), which helps define the widely used TL strain. Should longfin be considered an allele of kcnh2a?