[7/8] We think morphogen signaling partly governs how clones partition tasks in gastruloid development. Adding Retinoic Acid to chimeric gastruloids caused clones to mix together, and inhibiting Nodal signaling disrupted propensity, even though clones stayed separated from one another.

[6/8] We integrated our lineage-tracing with spatial transcriptomics. Pure-clone gastruloids poorly organize marker gene expression. Combined-clone gastruloids have marker gene expression that is more comparably organized to bulk gastruloids.

[3/8] Mixing clones together also helps gastruloids elongate properly, and again, each clone takes its preferred spot along the anterior-posterior axis, effectively partitioning the job of making the gastruloid among themselves.

[2/8] Every clone has a preferred location in the chimeric gastruloid. Some have a propensity for the anterior, some for the posterior. Here, that propensity held in nearly every gastruloid over several rounds of aggregation.

[1/8] We used a fluorescence-based lineage tracing approach to track individual clones in a polyclonal aggregate. Pure clones are worse at forming gastruloids. But crazily enough, if you mix them with the original bulk population, they do great!