The Dictyostelium genome encodes only two MAPKs, Erk1 and Erk2, and both are expressed during growth and development. Reduced levels of Erk2 expression have been shown previously to restrict cAMP production during development but still allow for chemotactic movement. In this study the erk2 gene was disrupted to eliminate Erk2 function. The absence of Erk2 resulted in a complete loss of folate and cAMP chemotaxis suggesting that this MAPK plays an integral role in the signaling mechanisms involved with this cellular response. However, folate stimulation of early chemotactic responses, such as Ras and PI3K activation and rapid actin filament formation, were not affected by the loss of Erk2 function. The erk2⁻ cells had a severe defect in growth on bacterial lawns but assays of bacterial cell engulfment displayed only subtle changes in the rate of bacterial engulfment. Only cells with no MAPK function, erk1⁻erk2⁻ double mutants, displayed a severe proliferation defect in axenic medium. Loss of Erk2 impaired the phosphorylation of Erk1 in secondary responses to folate stimulation indicating that Erk2 has a role in the regulation of Erk1 activation during chemotaxis. Loss of the only known Dictyostelium MAPK kinase, MekA, prevented the phosphorylation of Erk1 but not Erk2 in response to folate and cAMP confirming that Erk2 is not regulated by a conventional MAP2K. This lack of MAP2K phosphorylation of Erk2 and the sequence similarity of Erk2 to mammalian MAPK15 (Erk8) suggest that the Dictyostelium Erk2 belongs to a group of atypical MAPKs. MAPK activation has been observed in chemotactic responses in a wide range of organisms but this study demonstrates an essential role for MAPK function in chemotactic movement. This study also confirms that MAPKs provide critical contributions to cell proliferation.

该盘基网柄基因组编码只有两个的MAPK，ERK1和ERK2，和经济增长和发展的过程中表示。先前已证明Erk2表达水平降低会限制发育过程中的cAMP产生，但仍允许趋化运动。在这项研究中，erk2基因被破坏以消除Erk2功能。Erk2的缺乏导致叶酸和cAMP趋化性的完全丧失，表明该MAPK在与这种细胞应答有关的信号传导机制中起着不可或缺的作用。但是，叶酸刺激早期趋化反应，如Ras和PI3K活化和快速肌动蛋白丝形成，不受Erk2功能丧失的影响。该ERK2 ^-细胞在细菌草坪上的生长有严重缺陷，但是对细菌细胞吞噬的测定仅显示了细菌吞噬速率的细微变化。只有没有MAPK功能，细胞ERK1 ^- ERK2 ^-双突变体，显示在无菌介质中的严重缺陷扩散。Erk2的丧失削弱了对叶酸刺激的次级反应中Erk1的磷酸化，表明Erk2在趋化性过程中对Erk1激活的调节中具有作用。唯一已知的盘基网柄菌的丢失MAPK激酶MekA响应叶酸和cAMP阻止了Erk1的磷酸化，但阻止了Erk2的磷酸化，这证实了Erk2不受常规MAP2K的调控。Erk2的MAP2K磷酸化的缺乏和Erk2与哺乳动物MAPK15（Erk8）的序列相似性表明，网柄菌Erk2属于一组非典型MAPKs。在许多生物体的趋化反应中均已观察到MAPK激活，但这项研究表明MAPK功能在趋化运动中起着至关重要的作用。这项研究还证实了MAPK对细胞增殖提供了关键的作用。