Based on the fitness measurements, PCD benefits both species. Since PCD is clearly not beneficial to the actor, this study supports the argument that the phenomenon is an altruistic adaptation at a level of organization other than the individual cell. Our data show that PCD may be beneficial for population growth in nutrientlimited environments; however there may be other reasons not explored here. For example cellular aging or population regulation as well as non-adaptive pleiotropy or epistasis may make as yet undiscovered contributions. On a grander scale, by mediating such interplay with archaea and other organisms, diurnally synchronized cell death of algae is potentially an important determinant of microbial diversity and dynamics, succession of species, and biogeochmical cycles of C, N and P in natural aquatic ecosystems. As such, it also offers a new dimension to the structure of interspecies interactions in the microbial loop by adding to the diversity of mechanisms by which microbial interactions can occur. By characterizing the microbial loop in this manner we can now explore new strategies for predicting and managing the flux of C, N and other key elements of life with artificial or natural modulators of algal cell death. Such strategies could also have interesting biotechnology applications to the controlled harvest of algal products. Ironically, programmed death takes center stage in the complexity of a living system that is the microbial loop. The HER3 receptor is part of the epidermal growth factor receptor family, which is a group of tyrosine kinase receptors that mediate normal cellular functions such as proliferation and cell-tocell interactions, but have also been recognized as drivers of many different human cancers. Interestingly, HER3 differs from the other receptors 
of this family due to its inactive tyrosine kinase domain and hence, signals via ligand-induced heterodimer formation with other tyrosine kinase receptors. The HER2HER3 signaling pair is an oncogenic unit in many HER2-driven breast cancers and upregulation of the HER3 receptor has been shown to play a role in resistance to several currently approved drugs. Moreover, the importance of HER3 in human cancers is not limited to HER2-driven breast cancers, and HER3 has also been shown to be involved in for example tumorigenicity of HER3-overexpressing prostate cancer xenografts in vivo, to maintain in vivo proliferation of a subset of Amikacin hydrate ovarian cancers via an autocrine signaling loop, and to be involved in endocrine resistance of ER+breast cancer cell lines. Altogether, these findings demonstrate the potential of the HER3signalling pathway as an important therapeutic target in human cancers and several anti-HER3 antibodies are currently under clinical investigations. Recently, we have generated HER3-specific Affibody molecules of subnanomolar affinities, and demonstrated anti-proliferative attributes of these binders through blockage of ligand-induced HER3-signalling in vitro. These Chloroquine Phosphate growth-inhibitory effects were demonstrated to be a result of competitive HER3-binding between the Affibody molecules and the ligand heregulin. The small and cysteine-free three-helical Affibody molecules are straightforward to further modify by conjugations and fusions, for example when developing multispecific targeting molecules. In a recent study, Barbas and co-workers investigated this strategy using one of the HER3-specific Affibody molecules previously described by us. The Affibody molecule was fused with Cetuximab in order to generate a bispecific antibody targeting both EGFR and HER3.