Biology

The endosymbiont hypothesis offers an explanation for how eukaryptoc cells could have obtained mitochondria and chloroplasts through a symbiotic relationship with prokaryotic cells that changed over time. What structural feature of prokaryotic cells might you expect to have changed before any endosymbionts could be aquired by eukaryotic cells?

For some odd reason, I am kind of stuck on this question... would it be their cell walls?



Being as mitocondria and chloroplasts do not have cell walls it seems a reasonable answer. The paregraph below is copied from Wikipedia:

Around the outside of the cell membrane is the bacterial cell wall. Bacterial cell walls are made of peptidoglycan (called murein in older sources), which is made from polysaccharide chains cross-linked by unusual peptides containing D-amino acids.[4] Bacterial cell walls are different from the cell walls of plants and fungi which are made of cellulose and chitin, respectively.[5] The cell wall of bacteria is also distinct from that of Archaea, which do not contain peptidoglycan. The cell wall is essential to the survival of many bacteria and the antibiotic penicillin is able to kill bacteria by inhibiting a step in the synthesis of peptidoglycan.[5]

There are broadly speaking two different types of cell wall in bacteria, called Gram-positive and Gram-negative. The names originate from the reaction of cells to the Gram stain, a test long-employed for the classification of bacterial species.[6]

Gram-positive bacteria possess a thick cell wall containing many layers of peptidoglycan and teichoic acids. In contrast, Gram-negative bacteria have a relatively thin cell wall consisting of a few layers of peptidoglycan surrounded by a second lipid membrane containing lipopolysaccharides and lipoproteins. Most bacteria have the Gram-negative cell wall and only the Firmicutes and Actinobacteria (previously known as the low G+C and high G+C Gram-positive bacteria, respectively) have the alternative Gram-positive arrangement.[7] These differences in structure can produce differences in antibiotic susceptibility, for instance vancomycin can kill only Gram-positive bacteria and is ineffective against Gram-negative pathogens, such as Haemophilus influenzae or Pseudomonas aeruginosa.[8]

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