The previously accepted model of the chloramphenicol action was that it inhibited all ribosomes equally. Why were the authors of the Marks, 2016 paper skeptical of this model? Choose all that are...

Extracted text: The previously accepted model of the chloramphenicol action was that it inhibited all ribosomes equally. Why were the authors of the Marks, 2016 paper skeptical of this model? Choose all that are correct. Because they had observed that certain bacteria were resistant to chloramphenicol, and this proves that chloramphenicol stalls ribosomes at certain sites within those bacteria. Because certain MRNA templates had been observed to be inhibited by chloramphenicol more strongly than others Because chloramphenicol induces expression of chloramphenicol resistance proteins through translational arrest at specific codons in the leader ORFS of chloramphenicol resistance genes, which suggests there is preferential stalling at certain sites. Because chloramphenicol induces expression of chloramphenicol resistance proteins - therefore, these proteins must be able to be translated during chloramphenicol treatment. Because chloramphenicol binds the decoding center of the 30S subunit, and there are always different tRNAS there, which could interact with chloramphenicol differently.