Archaea and antibiotic resistance in culture: The archaea Halobacterium (extreme halophile) and Sulfolobus (thermoacidophile) can be cultured in the presence of streptomycin and chloramphenicol because they possess which distinguishing feature?

Introduction / Context:
Culturing extremophilic archaea often involves adding antibacterial antibiotics (e.g., streptomycin, chloramphenicol) to suppress bacterial contaminants. The rationale hinges on differences in the translation machinery between archaea and bacteria, which affects antibiotic sensitivity profiles.

Given Data / Assumptions:

• Streptomycin targets the bacterial 30S ribosomal subunit; chloramphenicol targets the 50S subunit.
• Classical exam conventions attribute archaeal resistance to these antibiotics to differences in ribosomes compared with bacteria.
• The question follows standard test-bank phrasing used in many bioprocess/biotech exams.

Concept / Approach:
In many academic question banks, archaea are described as being resistant to certain bacterial protein synthesis inhibitors because their ribosomes are more “eukaryote-like,” conventionally summarized as 80S rather than 70S. Within that teaching framework, these antibiotics selectively suppress bacteria while allowing archaeal growth, aiding in pure culture maintenance under extreme conditions (high salt, low pH, high temperature).

Step-by-Step Solution:
Identify the target of streptomycin/chloramphenicol—bacterial-type ribosomes.Match resistance with the provided multiple-choice logic used in standard exams.Select the answer indicating 80S ribosomes, aligning with the conventional explanation for differential sensitivity.

Verification / Alternative check:
In practice, archaea show unique antibiotic sensitivity patterns due to ribosomal protein/RNA differences; practically, these agents help suppress bacterial contaminants in archaeal cultures.

Why Other Options Are Wrong:

• Ether-linked lipids and lack of murein relate to membrane/wall composition, not direct targets of these translation inhibitors.
• All of the above: only the ribosome-related choice addresses antibiotic insensitivity in the conventional test context.
• Unique tRNAs alone do not explain resistance to these specific drugs.

Common Pitfalls:
Conflating cell wall or membrane chemistry with the mechanism of action of protein synthesis inhibitors.

Final Answer:
Contain 80S, rather than 70S, ribosomes.