Question of the week_2 Mar

Additional Misconception
Other Molecules that enter the Mitochondria:
NADH and FADH2

NOTE:
In oxidative phosphorylation, the NADH and FADH2 needed have two sources: from glycolysis in the cytosol and Krebs cycle in the matrix.

NADH from glycolysis has its electrons and protons shuttle across the the double membrane via shuttle systems to the FAD and NAD+ in the matrix, to reduce them to FADH2 and NADH respectively. The NADH does not transverse across the double membrane.

Nonetheless, the main bulk of FADH2 and NADH are formed in the matrix when pyruvate from glycolysis enters the matrix to undergo Krebs cycle.

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Was it Unclear?

Intracellular signalling is a complicated affair. We can spend weeks on it discussing the various receptors for different ligands and the different intracellular molecules involved for each. So apologies if things do get fuzzy but I will try my best to clear the air.

J asked about the need for a relay molecule to induce a signaling cascade. (as shown in notes)
Is it true for both types of receptors?

Yes.
The term ‘relay molecules’ is really a very generic one. Any molecules in the cascade can be considered a relay molecule.
However there was an attempt to differentiate the kinases and other proteins that are readily activated by the receptors.
When receptors are activated, as an immediate follow up, they can either activate a kinase directly or a non-kinase intermediate like G-proteins and your second messengers e.g. cAMP or even a docking protein (not taught) thus to simplify matters for both types of receptors, the term ‘relay molecule’ is coined instead.

Thus it is perfectly fine to say the receptors will activate a relay molecule which will trigger off a phosphorylation cascade by kinases (in the generic sense) unless you know the exact mechanism like for example the well-known G-protein-adenylyl cylase-protein kinase A pathway or any even given pathway.


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Evolution Baggage

Why do we call Photorespiration an Evolution Baggage?

The question arises because oxygen can compete with carbon dioxide for Rubisco and in so doing, reduce the efficiency of hexose sugar formation via the Calvin cycle as an alternative pathway (photorespiration) is engaged to produce glycolate and glycerate phosphate from RuBP instead, with the release of CO2 and consumption of ATP.

So where does the evolution part come in?
According to the hypothesis, eons ago, the atmosphere is made up of more CO2 and less O2, so carbon dioxide does not face much competition from oxygen for Rubisco so there was no strong selection pressure for a Rubisco that would exclude O2 from its active site. But as the O2 proportion in our atmosphere increase with respect to CO2, the rubisco still retains its chance affinity for O2 and thus perform photorespiration which makes carbon fixation less efficient.

Question: In that case, why doesn’t Rubisco co-evolve to only bind to carbon dioxide?
We are not too sure at the moment and we do not know if Rubisco can be beneficiall to the plants in other ways.
But some plants have attempted to overcome the problem with alternative pathways. To know more, google C4 plants and CAM plants. =)

On the same train of thought….glycolysis is actually a good old way to generate ATP.

Why oxygen is scarce in the eons-old past, early prokaryotes generates ATP exclusively from glycolysis which does not require oxygen. In fact, glycolysis is the most widespread metabolic pathway, suggesting its important role in the early history of earth. It being in the cytosol also play tribute to its historical past before the symbosis of prokaryotes to generate membrane-bound organelles in eukaryotes.