Daily Archives: July 30, 2018

Mitochondrial interactions with RER

Electron micrographs of liver, Glutamate cysteine ligase catalytic subunit KO mice, Mitochondria: electron microscopy, Ultimate order, the cell

Hepatocyte here, GCLC ko mouse, shows the donut and irregular configuration that is common in circumstances where mitochondria are stressed (I personally have seen it several times but in unrelated experimental circumstances so it is probably a generic response mostly).  In this really opportune section one can see a mitochondrion (with an odd donut shape) ont eh left, and a section of RER which has been sectioned tangentially showing the closeness and absolute regularity of the ribosomes along a spiral of mRNA.

I bet at some point all information about these association and the proteins (i saw a list that mentioned in the 800s and counting) in the inner and outer and cristae membranes, and the cristae junctions as well as the matrix will be modeled.  Until then, circumstantial evidence for the power of the interactions between mitochondria and other organelles (and cytoskeletal proteins) has to suffice.

The ribosome spirals here look to have approximately 7.3+/- .47 (SEM) ribosomes per spiral, n=9 (a small sample but the best orientation, and a single micrograph…. so this is just a suggested number obviously.  19735_73218_#201 liver alb+/- Gckc -/- postnatal day 28. liver mouse, no NAC.

One thing abou these mice that is pneumonic is the dilated ER, a mix of smooth and rough, ribosomes spaced and the presence of the little bubble-blip invaginations of ER within the outer RER membranes.  These mitochondria also display fission lines and tubular cristae, and quite a bit of it.  Blue dotted line (outline of one part of a mitochondrion – that one tangentially sectioned beside the RER, white box, area for enlargement to the right. Upper image on right has cytoplasmic ribosomes in mRNA-spirals (orange) and lower image is contrast enhanced to highlight the spirals of cytoplasmic ribosomes.  I really don’t think there are any good examples of mitoribosomes in either of the two mitochondria shown here.

Numerous proteins in the outer mitochondrial membrane (encoded by nuclear DNA) target and or are attached to cytoplasmic ribosomes. Cytoplasmic ribosomes have been visualized on mitochondria membranes (that would be the cytoplasmic face of the OMM). These are suggested to be linked by the translocase of the (outer) mitochondrial membrane (TOM) and it is reported that the ribosomes are in clusters (Till Klecker et al, 2014 Trends in Cell Biology) and that pretty much looks like these nRNA-ribosomal spirals… tidily wound.

MDVs, mitochondrially derived vesicles (about 70-150nm) are  purposeful buds of membrane derived from mitochondria which are targeted to lysosomes, and maybe other organelles.

Just an “aside” here, but is it possible that the donut shaped mitochondria (invaginations, and extra turns and indents) might be somehow a deliberate attempt to increase surface area for interaction with other membranes.   Another question is the orientation of cristae.  I have looked for cristae pores, and that relationship…  just not seeing it overtly.

Different effects from different types of trauma

Lichen planus

I have casually logged into my mind what kinds of trauma to the skin turn into lichen planus lesions and which do not.  For starters, it seems that trauma from items which have antigenic properties (eg cat scratch, dog toenail scrapes, rubbing from a dog leash over the wrists) become real lichen planus lesions, where as more sterile injuries, bumps, pin pricks (as in sewing) dont have the same tendencies.  Another mystery is why “on me anyway” spider bites (1/2 inch red area with swelling and a central darker dot) don’t turn into lichen planus lesions.

I had a biopsy of a 30 or 40 year old lesion on my leg that was left over from small pox vaccination (which at that point in time was a conventional remedy for apthous ulcers, since it was believed there was some cross immunity achieved — that is not done any more, but because other herpes type viruses  can show post-infection increase in lichen planus i will be curious to see if that pathology matches others taken in my case.

Also noted, the impact of chemicals as instigators of lesions at points of trauma seems to be prevalent, eg, bandage adhesives.

While this disease requires the utmost of patience, and heroic efforts are required to keep from scratching, maybe there is healing somewhere for some people and at some point treatments will be found…. likely like one will have to say… I am a “recovering” lichen planus patient, as i don’t think the basic predispositions may be only genetic (as writen in genetic code or epigenetic modifications)  ha ha.  or not so ha ha but has an environmental (environment in the greatest sense that includes, chemicals, irritant compounds, man made compounds, diet, stress and the whole nine yards).  My sympathies to all you out there with this disorder. What is clear that diseases processes and problems that don’t threaten “life” get sent to the back burner in terms of research.

Mitochondrial proteins in membranes at desmosomal tethers

Desmosomal mitochondrial associations

This concept of organellar interaction is of course old, and even has been on my mind for decades. I have made many posts on the tethers seen between mitochondria and desmosomes and hope at some point to understand and diagram the relevant collection of outer and inner mitochondrial membrane proteins (black lines above the membranes show area in question) present at the points of attachments to the intermediate filaments (red line shows direction) of desmosomal mitochondrial tethering. Box in top figure is rotated and enlarged for inset. Rat #9, liver 5983,  BH