Scholarlink

Background <p>When starved, <i>Dictyostelium discoideum</i> cells form clusters that, when constrained in height, exhibit clear collective rotational motion. During this collective rotation, cells secrete and relay the chemoattractant cAMP, resulting in signal propagation in the form of spiral waves, which rotate in the opposite direction of the collective rotation. The quantification of this collective rotation with reference to cAMP signaling and the dependence on cluster size is currently unclear.</p> Results <p>In this study, we use experiments and modeling to investigate how cell motion and cAMP signaling dynamics depend on cluster sizes in <i>Dictyostelium</i> using aggregates that are confined to quasi-2D environments. For rotating clusters with a single cAMP spiral arm, we find that both cAMP wave and cell angular velocities decrease as cluster sizes increase, suggesting that larger clusters signal more slowly. We also show that the angular velocity of the cells (<InlineEquation ID="IEq1"><EquationSource Format="TEX">\(\omega_{\text{cell}}\)</EquationSource></InlineEquation>) is linearly correlated with the angular velocity of the cAMP wave (<InlineEquation ID="IEq2"><EquationSource Format="TEX">\(\omega_{\text{wave}}\)</EquationSource></InlineEquation>). For clusters with multiple spiral arms, we observe a size dependence where larger clusters have a higher probability of having more spiral arms compared to smaller clusters. The qualitative experimental results are consistent with a computational model that couples a reaction diffusion model to cell motility and chemotaxis. Our simulation results suggest that a variable degradation rate of cAMP, which depends on cluster size, is a possible mechanism to explain the cluster size-dependent wave and cell angular velocities.</p> Conclusion <p>Together, these findings identify cluster size as a key regulator of both cAMP wave dynamics and collective cell motion and link slower signaling and enhanced multi-armed spiral formation to larger clusters. More broadly, our work suggests that size-dependent modulation of extracellular cAMP degradation can couple cell number to emergent spatiotemporal patterns in developing <i>Dictyostelium</i> aggregates.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

From microscope to model: rotating signaling dynamics and cluster size in Dictyostelium discoideum aggregates

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月3日

查看全文
  • Sanchi Saitia,
  • Yi-Chieh Lai,
  • Man-Ho Tang,
  • Jasper Jain,
  • Michael Reiss,
  • Wouter-Jan Rappel

摘要

Background

When starved, Dictyostelium discoideum cells form clusters that, when constrained in height, exhibit clear collective rotational motion. During this collective rotation, cells secrete and relay the chemoattractant cAMP, resulting in signal propagation in the form of spiral waves, which rotate in the opposite direction of the collective rotation. The quantification of this collective rotation with reference to cAMP signaling and the dependence on cluster size is currently unclear.

Results

In this study, we use experiments and modeling to investigate how cell motion and cAMP signaling dynamics depend on cluster sizes in Dictyostelium using aggregates that are confined to quasi-2D environments. For rotating clusters with a single cAMP spiral arm, we find that both cAMP wave and cell angular velocities decrease as cluster sizes increase, suggesting that larger clusters signal more slowly. We also show that the angular velocity of the cells (\(\omega_{\text{cell}}\)) is linearly correlated with the angular velocity of the cAMP wave (\(\omega_{\text{wave}}\)). For clusters with multiple spiral arms, we observe a size dependence where larger clusters have a higher probability of having more spiral arms compared to smaller clusters. The qualitative experimental results are consistent with a computational model that couples a reaction diffusion model to cell motility and chemotaxis. Our simulation results suggest that a variable degradation rate of cAMP, which depends on cluster size, is a possible mechanism to explain the cluster size-dependent wave and cell angular velocities.

Conclusion

Together, these findings identify cluster size as a key regulator of both cAMP wave dynamics and collective cell motion and link slower signaling and enhanced multi-armed spiral formation to larger clusters. More broadly, our work suggests that size-dependent modulation of extracellular cAMP degradation can couple cell number to emergent spatiotemporal patterns in developing Dictyostelium aggregates.