Final answer:
The lack of ill effects in mice lacking the kinesin gene suggests that there are other compensatory or redundant systems in place, such as alternative motor proteins that can fulfill the role of kinesin in intracellular transport.
Step-by-step explanation:
If a mouse lacking copies of the conventional kinesin gene shows no ill effects and lives a normal lifespan, one might conclude that there are redundant mechanisms in place for intracellular transport, or that other motor proteins can compensate for the absence of kinesin. It is known that motor proteins are crucial for the transport of cellular materials, such as organelles, vesicles, and neurotransmitters, particularly along microtubules. Kinesin typically moves cargo towards the plus-end of microtubules, often from the cell body to the periphery, a process known as anterograde transport.
Sometimes organisms can adapt to gene loss by utilizing alternative pathways or proteins. For instance, the motor protein dynein moves cargo in the opposite direction (retrograde transport) and could potentially take over some functions normally attributed to kinesin. Since mice without kinesin can live normally, it suggests a surprising flexibility in cellular transport systems, possibly due to compensatory functions from other motor proteins or redundancy within the system. This could prompt further research into the plasticity of intracellular locomotion mechanisms.