Fig. 6

Scheme of HCF101 evolution. A. HCF101 distribution explained via the Chromalveolate hypothesis. Upon the acquisition of HCF101-like protein via LGT from bacteria to the ancestor of Archeplastida, chHCF101 was established in the plastid. Euglenozoa gained HCF101 via secondary endosymbiosis with a donor containing green plastid. A common ancestor of Chromalveolata gained red plastid via secondary endosymbiosis, the gene for chHCF101 was duplicated and one copy was targeted to mitochondria (mHCF101), where it replaced the Ind1 gene. mHCF101 is common to all chromalveolates, while several lineages lost chHCF101 together with loss of the secondary plastid (Cryptosporidium, Ciliates, Oomycota, centrohelids, catablepharids). B. HCF101 distribution explained via ‘multiple secondary endosymbiosis’. Mitochondrially localized HCF101 together with Ind1 was present in a common ancestor of Archaeplastida, SAR, Cryptista, and Haptista. Then, in (i) Cryptista and in (ii) a common ancestor of Haptista and SAR, the Ind1 gene was lost, whereas the Archaeplastida gene for the Ind1 protein remained in the mitochondria, and mHCF101 was retargeted to the plastid. Then, chHCF101 was introduced to Cryptophytes, Haptophytes, and certain SAR groups via multiple secondary endosymbiosis. chHCF101 is absent in lineages that did not experience secondary endosymbiosis. The schematic tree is based on previous phylogenetic studies [29, 31, 32, 36, 47, 53, 99]. PR, protein retargeting; GL, gene loss; GD, gene duplication; PL, plastid loss; PES, primary endosymbiosis; SES, secondary endosymbiosis; TES, tertiary endosymbiosis