Editing Symbiogenesis (section)

== Organellar genomes ==

=== Plastomes and mitogenomes ===

[[File:Map of the human mitochondrial genome.svg|thumb|upright=1.5|The [[Human mitochondrial genetics|human mitochondrial genome]] has retained genes encoding 2 [[rRNA]]s (blue), 22 [[tRNA]]s (white), and 13 redox [[protein]]s (yellow, orange, red).]]

Some endosymbiont genes remain in the organelles. Plastids and mitochondria retain genes encoding rRNAs, tRNAs, proteins involved in redox reactions, and proteins required for transcription, translation, and replication. There are many hypotheses to explain why organelles retain a small portion of their genome; however no one hypothesis will apply to all organisms, and the topic is still quite controversial. The hydrophobicity hypothesis states that highly [[hydrophobic]] (water hating) proteins (such as the membrane bound proteins involved in [[redox]] reactions) are not easily transported through the cytosol and therefore these proteins must be encoded in their respective organelles. The code disparity hypothesis states that the limit on transfer is due to differing genetic codes and RNA editing between the organelle and the nucleus. The redox control hypothesis states that genes encoding redox reaction proteins are retained in order to effectively couple the need for repair and the synthesis of these proteins. For example, if one of the [[photosystem]]s is lost from the plastid, the intermediate electron carriers may lose or gain too many electrons, signalling the need for repair of a photosystem. The time delay involved in signalling the nucleus and transporting a cytosolic protein to the organelle results in the production of damaging [[reactive oxygen species]]. The final hypothesis states that the assembly of membrane proteins, particularly those involved in redox reactions, requires coordinated synthesis and assembly of subunits; however, translation and protein transport coordination is more difficult to control in the cytoplasm.<ref name="Timmis2004"/><ref name="LilaKoumandou2004"/><ref name="Barbrook2006"/><ref>{{Cite journal |last1=Giannakis |first1=Konstantinos |last2=Arrowsmith |first2=Samuel J. |last3=Richards |first3=Luke |last4=Gasparini |first4=Sara |last5=Chustecki |first5=Joanna M. |last6=Røyrvik |first6=Ellen C. |last7=Johnston |first7=Iain G. |display-authors=3 |date=16 September 2022 |title=Evolutionary inference across eukaryotes identifies universal features shaping organelle gene retention |journal=Cell Systems |volume=13 |issue=11 |pages=874–884.e5 |doi=10.1016/j.cels.2022.08.007 |pmid=36115336|s2cid=252337501 |doi-access=free |hdl=11250/3045694 |hdl-access=free }}</ref>

=== Non-photosynthetic plastid genomes ===

The majority of the genes in the mitochondria and plastids are related to the expression (transcription, translation and replication) of genes encoding proteins involved in either photosynthesis (in plastids) or cellular respiration (in mitochondria). One might predict that the loss of photosynthesis or cellular respiration would allow for the complete loss of the plastid genome or the mitochondrial genome respectively.<ref name="Timmis2004"/><ref name="LilaKoumandou2004"/><ref name="Barbrook2006"/> While there are numerous examples of mitochondrial descendants ([[mitosome]]s and [[hydrogenosome]]s) that have lost their entire organellar genome,<ref name="Howe2008">{{cite journal |last=Howe |first=Christopher J. |title=Cellular evolution: what's in a mitochondrion? |journal=Current Biology |volume=18 |issue=10 |pages=R429–R431 |date=May 2008 |pmid=18492476 |doi=10.1016/j.cub.2008.04.007 |s2cid=15730462 |doi-access=free |bibcode=2008CBio...18.R429H }}</ref> non-photosynthetic plastids tend to retain a small genome. There are two main hypotheses to explain this occurrence:<ref name="Barbrook2006"/><ref name="Lane2011"/>

The essential tRNA hypothesis notes that there have been no documented functional plastid-to-nucleus gene transfers of genes encoding RNA products (tRNAs and rRNAs). As a result, plastids must make their own functional RNAs or import nuclear counterparts. The genes encoding tRNA-Glu and tRNA-fmet, however, appear to be indispensable. The plastid is responsible for [[heme|haem]] biosynthesis, which requires plastid encoded tRNA-Glu (from the gene trnE) as a precursor molecule. Like other genes encoding RNAs, trnE cannot be transferred to the nucleus. In addition, it is unlikely trnE could be replaced by a [[cytosol]]ic tRNA-Glu as trnE is highly conserved; single base changes in trnE have resulted in the loss of haem synthesis. The gene for tRNA-[[N-Formylmethionine|formylmethionine]] (tRNA-fmet) is also encoded in the plastid genome and is required for translation initiation in both plastids and mitochondria. A plastid is required to continue expressing the gene for tRNA-fmet so long as the mitochondrion is translating proteins.<ref name="Barbrook2006"/>

The limited window hypothesis offers a more general explanation for the retention of genes in non-photosynthetic plastids.<ref name="Lane2011">{{cite journal |last=Lane |first=Nick |author-link=Nick Lane |title=Plastids, genomes, and the probability of gene transfer |journal=Genome Biology and Evolution |volume=3 |pages=372–374 |date=2011 |pmid=21292628 |pmc=3101016 |doi=10.1093/gbe/evr003 }}</ref> According to this hypothesis, genes are transferred to the nucleus following the disturbance of organelles.<ref name="Leister2005"/> Disturbance was common in the early stages of endosymbiosis, however, once the host cell gained control of organelle division, eukaryotes could evolve to have only one plastid per cell. Having only one plastid severely limits gene transfer<ref name="Barbrook2006"/> as the lysis of the single plastid would likely result in cell death.<ref name="Barbrook2006"/><ref name="Lane2011"/> Consistent with this hypothesis, organisms with multiple plastids show an 80-fold increase in plastid-to-nucleus gene transfer compared with organisms with single plastids.<ref name="Lane2011"/>