They're very similar! Explanation: The major difference between meiosis II and mitosis is the ploidy of the starting cell. Meiosis II begins with two haploid cells, which have half the number of chromosomes as somatic cells. This is because they will develop into gametes.
Mitosis begins with a diploid cell. It will divide into two sister cells, both of which are also diploid. Related questions How do I determine the molecular shape of a molecule?
The radial array of microtubules is not evident in cells at mitotic onset, in which kinetochores are constantly located in the vicinity of SPBs. When kinetochores are artificially detached from SPBs upon entry into mitosis, for example, by the use of transient exposure to microtubule poisons, similar long microtubules are assembled after drug washout to capture and collect the scattered kinetochores. Thus, the machinery utilizing extending microtubules may also operate during mitosis as a backup system to respond to the unexpected risk, although it has not been clarified if the molecular mechanisms for microtubule extension are identical in mitosis and in meiosis.
Alternatively, either SPB separation or maturation in meiosis I could be repressed by slim SPBs during meiotic prophase to efficiently form a radial microtubule array. In meiosis, however, extension of microtubules is observed in cells at the stage without exception, and the microtubules complete kinetochore retrieval mostly by the time SPBs start to separate Figures 2F,G , suggesting that the scheme in meiosis is programmed as a physiological system rather than as a reflex action to the contingency.
The second strategy, namely, the precocious deposition of Alp7 to microtubule-free kinetochores, is exclusively observed in this stage, and a similar localization cannot be observed in mitotic cells. Thus, deposition of Alp7 to pre-attached kinetochores is programmed specifically for meiosis. This is indeed evidenced by the molecular mechanism underlying the precocious localization of Alp7 to meiotic kinetochores: the meiosis-specific localization of Alp7 is dependent on the Polo kinase Plo1, which is also located to pre-attached kinetochores in meiosis Figure 2D.
As mentioned above, Plo1 localizes to pre-attached kinetochores using Moa1 Meikin as a platform; therefore, Alp7 localization to the kinetochores is also a meiosis-specific event. Taken together, we consider that Moa1—Plo1 plays the third function in meiosis—at the onset of meiosis I, kinetochores are highlighted as center for microtubule control: Moa1 Meikin recruits Plo1 Polo kinase , which deposits Alp7 TACC to stably capture microtubules emanated radially from spindle poles.
Moa1—Plo1 has an additional role: Plo1 at meiotic kinetochores also phosphorylates Spc7 KNL1 of the outer kinetochore components. This affects the localization of Bub1 kinase which is known as a checkpoint kinase and phosphorylates histone H2A to recruit shugoshin at centromeres Tang et al.
In mitosis, the kinetochore localization of Bub1 is transient, whereas Bub1 in meiosis persists at kinetochores until anaphase of meiosis I because Spc7, the platform for Bub1, is phosphorylated by Plo1 specifically in meiosis Miyazaki et al.
Thus, Moa1—Plo1 plays a central role to dictate a number of meiosis-specific events regarding the interaction of kinetochores and microtubules, thereby differentiating meiosis from mitosis. The progression of kinetochore—microtubule association is monitored by the spindle assembly checkpoint SAC machinery in mitosis and meiosis. Briefly, kinetochores unattached to microtubules are recognized by the Mad1—Mad2 complex, the main components of SAC.
When chromosomes are repositioned at the onset of meiosis I, the unattached kinetochores are not recognized by Mad1—Mad2. This is probably due to a lack of sufficient CDK activity, which is a prerequisite for the localization of Mad1—Mad2 to unattached kinetochores Aoi et al. For an entire resolution of the bouquet arrangement, telomeres that have been clustered around SPBs during meiotic prophase are detached from SPBs upon entry Figure 2E , although the molecular mechanism remains elusive.
Resolution of telomere clustering occurs almost at the same timing with kinetochore retrieval, albeit slightly later than the retrieval. The resolution requires elevation of the cyclin-dependent kinase activity by Cdc25 phosphatase, which is transcriptionally activated by the meiosis-specific transcription factor Mei4 Murakami-Tonami et al. Cdc13 cyclin B predominantly accumulates at bouquet telomeres for the resolution of telomere clustering Moiseeva et al. It has been recently shown that difference in chromosome configuration in mitosis and meiosis affects bipolar spindle organization using their kinetic properties.
The assembly of bipolar spindle is based on the elongation of microtubules and their mutual and physical interaction. Spindle microtubules are emanated from both of the two SPBs, and they interact with each other to separate the SPBs outward, which is the major driving force for bipolar spindle formation. As illustrated in Figure 3A , a couple of kinesin motor proteins are involved in the separation of two SPBs.
Kinesin-5 is a conserved subfamily of the kinesin superfamily motor proteins that move to plus-ends and functions as a homo-tetramer Hagan and Yanagida, , ; Kapoor et al.
Cut7, the fission yeast ortholog of kinesin-5 subfamily members, is an essential protein required for outward SPB separation that functions as a tetramer Hagan and Yanagida, , ; Akera et al. Cut7 captures the lateral surface of a pair of interpolar microtubules emanating from both SPBs, and it moves toward their plus-ends along the microtubules.
Figure 3. Force balance affects spindle pole body SPB separation in mitosis and meiosis. A tetramer of Cut7 red captures two bundles of microtubules. When they are aligned in an anti-parallel manner, the plus-end-directed Cut7 generates the outward force that consequently separates two SPBs. Microtubules are tethered to SPBs at their minus ends.
Pkl1 localizes to SPBs and Klp2 to the microtubules. Those minus-end-directed motors generate the inward force. B SPB separation in prometaphase of mitosis. D When Swi6 HP1 is deleted, the structure of sister kinetochores is loosened, which does not generate a sufficient repulsive force to separate SPBs. On the contrary, members belonging to another subfamily kinesin Pkl1 and Klp2 are minus-end-directed and generate inward forces for SPBs Figure 3A. Pkl1 preferentially localizes to SPBs and the spindle as well as the nucleoplasm during mitosis, and Klp2 localizes to spindle microtubules Pidoux et al.
In the absence of two antagonistic kinesins Cut7 and Pkl1, the outward force wins again to consequently separate the SPBs mitosis, Figure 3C. This also indicates that there are additional factors that generate the outward force to separate SPBs other than Cut7. One of such factors is the microtubule-associated protein Ase1 human PRC1 , which is known to connect a pair of interdigitating microtubules as an anti-parallel bundle Pellman et al.
Similarly, other microtubule-associated proteins promote outward force generation in the absence of Cut7 Yukawa et al. In addition to microtubule-associated proteins, chromosome is another factor that generates outward force for SPB separation. The microtubules use the sister kinetochores as the fulcrum to generate the repulsive force which separates SPBs.
This is evidenced by genetic analyses; for instance, SPB separation is inhibited when the mitotic cohesin Rad21 is removed i. Moreover, when the sister kinetochores are unfastened by reduction of centromeric cohesion using deletion of Swi6 HP1 Ekwall et al. These results altogether demonstrate that centromeric cohesion and functional sister kinetochores are required for generation of the outward force in the absence of Cut7 and Pkl1.
This is due to the loosened connection between homologous kinetochores instead of a tight sister kinetochore connection of mitotic cells Figure 3E. When mono-orientation of sister chromatids is converted to bi-orientation by deletion of Moa1 i. This provides us two concepts. First, the rigidity of the kinetochore connection matters because it determines whether an additional outward force for SPB separation is generated in mitosis and in meiosis.
Second, the kinetochore-mediated outward force is weaker in meiosis I than in mitosis, owing to meiotic kinetochore mono-orientation. This may lead to a delay in SPB separation in meiosis I, unless the Cut7-mediated force is somehow augmented or the opposing inward force by kinesin motors decreases. When kinetochores are retrieved to the close vicinity of SPBs, it may be able to generate a rigid repulsive force by short microtubules that is sufficient for SPB separation.
This may be reasonable for cells at this stage, as they need to earn some additional time until all the scattered kinetochores are collected to SPBs. Thus, the kinetochore-mediated repulsive force may modulate the balance of mechanical forces, through which meiosis-specific cell cycle progression and chromosomal events may be timely coordinated. In general, either in mitosis or meiosis, fission yeast microtubules do not complete end-on attachment to kinetochores by the timing of SPB separation.
Therefore, the kinetochore-mediated SPB separation may not rely on the end-on attachment; rather, a pair of bi-oriented kinetochores serves as a glue factor that connects two anti-parallel microtubules through attachment to their lateral surfaces, similarly to the microtubule-associated bundling factor Ase1. Kinetochore-driven centrosome separation has also been observed in HeLa cells. When a kinetochore protein, either CENP-O Mcm21 or CENP-L, is depleted, separation of centrosomes is delayed albeit partially, and this is due to defects in the formation of kinetochore microtubules kinetochore fibers or k-fibers Toso et al.
There are two major pathways for centrosome separation in HeLa mitosis: the aurora A-dependent pathway, which is presumably for centrosomal microtubule-mediated separation, and the kinetochore-dependent pathway Toso et al. When the nuclear envelope breakdown precedes centrosome separation in prometaphase, lateral attachment and kinetochores to microtubules and their lateral transport are promoted to form a ring-like alignment of chromosomes, called prometaphase rosette Nagele et al.
The prometaphase rosette is gradually converted to metaphase congression through the transport of laterally attached kinetochores by the kinesin-7 motor CENP-E and the chromokinesin Kid Tokai et al. Kinetochore-driven centrosome separation may occur during the conversion and establishment of the metaphase alignment. These observations imply that the way of kinetochore-mediated SPB separation is an analogous phenomenon to the similar centrosome separation.
During acentrosomal meiosis I of mouse oocytes, the Ndc80 complex of outer kinetochores accumulate the microtubule crosslinker Prc1 yeast Ase1 to kinetochores, which becomes a center for microtubule bundling to assemble the functional bipolar spindle even without positional cues at spindle poles Yoshida et al.
As mentioned above, the SAC machinery monitors the state of kinetochore—microtubule interaction, and in the case of problems, SAC arrests cell cycle progression in metaphase. SAC detects two types of erroneous interactions: an improper attachment and a lack of tension between kinetochores Nezi and Musacchio, The overall functions of SAC are common in mitosis and in meiosis, but tension is generated in a different manner.
In mitosis, tension by microtubules is generated between sister kinetochores left, Figure 1B , whereas it is generated between homologous kinetochores right.
In anaphase I, homologous chromosomes with chiasmata are segregated; hence, chiasmata need to be resolved by anaphase onset. SCF constitutes a conserved ubiquitin ligase family and contributes a number of cellular phenomena, and the fission yeast orthologs of the components are Skp1, Cul1, and at least 18 F-box proteins [reviewed in Toda et al. In the temperature-sensitive mutant of SCF—Skp1 skp1 -ts , the anaphase spindle becomes abnormally bent in the nucleus, both in mitotic and meiotic anaphase Lehmann and Toda, ; Okamoto et al.
The bend spindle in anaphase I is due to unresolved meiotic recombination intermediates that remained until anaphase as evidenced by the prolonged foci of Rad51 the RecA homolog indicating sites of meiotic recombination Muris et al.
When meiotic cohesin Rec8 or the meiotic endonuclease Spo11 the fission yeast ortholog is named Rec12 is deleted, the bent spindle phenotype is suppressed, verifying that entangled chromosomes by prolonged recombination intermediates attached to microtubules hamper the full elongation of the anaphase spindle; therefore, the spindle is bent.
In conclusion, Skp1 and the F-box helicase Fbh1 are required for the resolution of meiotic recombination intermediates, although it remains to be elucidated which protein is targeted by SCF-Skp1—Fbh1 for degradation for the resolution Okamoto et al.
The function of SCF—Skp1 in the resolution process appears conserved in eukaryotes: the Arabidopsis ask1 mutant Ask1 is the Skp1 ortholog has the spindle which displays an overall normal structure but somewhat longer than that of WT cells during meiosis I Yang et al. The difference in spindle morphology bent or long in these two organisms could be simply due to whether the spindle poles are embedded in the nuclear envelope and whether the spindle is assembled in the compartmentalized nucleus in closed mitosis Figure 4A , and the function in resolution of meiotic intermediates is likely to be conserved.
Figure 4. Meiosis-specific cell cycle progression from meiosis I to meiosis II. After anaphase I, only one of two nuclei is chosen for drawing to illustrate MII progression.
At the transition stage of metaphase to anaphase, each SPB is modified, and the globular forespore membrane FSM begins to grow to surround the nucleus. The leading edge of the FSM opening is decorated by leading edge proteins. During anaphase II, the barrier function of the nuclear envelope is invalidated, which is an incident called virtual nuclear envelope breakdown. After completion of MII, the rigid spore wall is assembled. B The kinetics of the CDK activity during meiosis.
The horizontal axis time is shared with the time scale in A. The cells then start the aberrant third division albeit incomplete. One of the most enigmatic mechanisms of meiosis is two consecutive rounds of cell division: meiosis I MI and meiosis II MII without replicating DNAs, which is a clear contrast to the single M phase per cell cycle in mitotically growing cells.
Specialized regulation of CDK is essential for the interkinesis period, followed by the initiation of meiosis II. The drug-sensitive mutant cdc2-as analog-sensitive Dischinger et al.
The cdc2-as mutant is deficient in meiosis II initiation and terminates meiosis in a binucleate state even without exposure to the ATP analog. The activity of the mutant protein can be regained by the introduction of a suppressor mutation into the Cdc2-as protein. The cdc2-asM17 mutant has additional mutations to improve the Cdc2-as activity and proceeds meiosis normally to produce normal spores Aoi et al.
In WT meiocytes, Slp1 is the main coactivator for anaphase I onset, whereas Fzr1 is mainly for anaphase II onset and completion of meiosis. Mes1 is a competitive substrate but not a pseudosubstrate for Slp1; therefore, Slp1 eventually overcomes the inhibition by Mes1 and triggers anaphase I onset Kimata et al. On the contrary, Mes1 serves as a pseudosubstrate for Fzr1; therefore, Fzr1 remains inactive possibly until Mes1 is somehow diminished. The activity of SAC during two sequential divisions may be regulated in a continuous manner.
When the first division is delayed by SAC, the anaphase onset of meiosis II is advanced, which means that the SAC effect was reduced at meiosis II to compensate the previous delay that occurred in meiosis I Yamamoto et al.
In conclusion, the number of meiotic divisions is exclusively determined as two, neither one nor three. Although the seesaw battle is commonly seen in meiocytes of any species, the underlying molecular mechanisms may be divergent.
The functional homologs of S. In oocyte meiosis of vertebrates, Erp1 functions as a cytostatic factor that arrests the meiotic cell cycle in metaphase II Masui and Markert, ; Inoue et al. Although the players for the CDK—APC seesaw battle appears conserved in fission yeast and plant cells, the way of molecular regulation seems distinct.
For meiotic exit, the active level of fission yeast Fzr1 may be regulated transcriptionally, but the plant TDM1 is post-translationally regulated through phosphorylation Cifuentes et al. The other S. Spo5 promotes progression of meiosis II through regulation of cyclin B Arata et al.
At the moment, the mes mutants isolated to date are only two, and many things still remain to be elucidated: e. It is reported that the mes1 gene is spliced only during meiosis Kishida et al.
Although the mechanism remains unclear, this may be dependent on the meiosis-specific splicing machinery particularly driven by the promoter region and transcription factors belonging to the forkhead family Averbeck et al. The second division of meiosis is similar to mitosis regarding the pattern of chromosome segregation equational division , in which sister chromatids are segregated.
Besides that, meiosis II is generally linked with gametogenesis, which corresponds to sporulation in yeast species. The detailed processes of sporulation and underlying molecular mechanisms are comprehensively reviewed in Shimoda ; therefore, here we briefly summarize the general picture of sporulation events. The forespore membrane gradually grows to surround and cover the nucleus from both SPBs, and the edge of the opening region of the forespore membrane is entirely decorated by the leading edge proteins LEPs including Meu14 Okuzaki et al.
Growth of the forespore membrane is guided by LEPs and septins over the anaphase nucleus, and the opening closes by contraction, thereby completely surrounding the divided nuclei Onishi et al. The hard spore wall is then formed after completion of the forespore membrane. Observations in the last decade revealed that the sporulation events give some unexpected impacts on the progression of meiosis II.
Here we focus on an interesting behavior of the nuclear envelope: virtual nuclear envelope breakdown vNEBD. Both S. In anaphase II, nucleoplasmic proteins mostly dispersed, although observation of the nuclear envelope and the nuclear pore complex indicated that the nuclear envelope itself is not particularly disrupted or fragmented at least in fluorescence microscopy and in transmission electron microscopy Arai et al.
One of the triggers of vNEBD in anaphase II may be related to the formation of the forespore membrane, which is also assembled at the same timing. The dispersal of nuclear proteins to the cytoplasm during anaphase II can be blocked in several spo gene mutants, which are involved in the assembly of the forespore membrane.
When the nuclear envelope expands in anaphase II, the lipid components constituting the nuclear envelope may be in a shortage because the components may need to be preferentially used for the assembly of the forespore membrane. This idea is based on the fact that vNEBD does not occur when the vesicle transport pathway that conveys membrane components from Golgi to endoplasmic reticulum is inhibited by a drug Arai et al.
This implies the possibility that vNEBD may be caused by a shortage of nuclear envelope components, which results in an increase of membrane permeability only during anaphase II. Even when the nuclear envelope seemingly persists as in closed meiosis II, the nuclear conditions can be temporarily neutralized as is seen in open mitosis of higher eukaryotes.
The biological roles of vNEBD had been undefined, but recently it was shown to promote the maturation of spores through redistribution of the nuclear proteasome subunit Rpn11 to the cytoplasm Yang et al.
This means that vNEBD can be induced by sporulation events, which in turn feedbacks to promote spore maturation. Further studies will illuminate the molecular mechanisms to trigger vNEBD as well as the biological significance of the phenomenon. As the interplay between the nuclear envelope and the genome contributes to the determination of cell fate [reviewed in Talamas and Capelson ], it would be tempting to investigate the role of v NEBD for differentiation of cells in yeast and other species.
Another unexpected aspect of sporulation events is the effect of the forespore membrane on the spindle of meiosis II. In general, the spindle comprises three types of microtubules: kinetochore microtubules kinetochore fibers, k-fibers as mentioned earlier see Figures 2C,G , interpolar microtubules connecting two spindle poles in an antiparallel manner, and astral microtubules extending outward of the spindle from the poles.
In fission yeast, the majority of astral microtubules are formed in the cytoplasm from SPBs, and some bundles are in the nucleus Zimmerman et al. Other two types are in the nucleus. Both kinetochore microtubules and interpolar microtubules are essential in mitosis and meiosis I, but interpolar microtubules are dispensable for the bi-directional segregation of chromosomes only in meiosis II Akera et al. When interpolar microtubules are disrupted by microtubule poisons, the globular forespore membrane serves as an interpolar structure on their behalf to separate SPBs to assemble a bipolar apparatus and to separate two nuclei.
The forespore membrane is guided by LEPs and septin proteins and grows from two SPBs, and two globular structures make a physical contact with each other in the middle of the nucleus in anaphase II, when the interpolar microtubules are destroyed by microtubule poisons. As a pair of the contacted forespore membrane grows, they gradually cleave and separate the anaphase nucleus into two, even though there is no spindle elongation in the conditions.
Data remained elusive on whether kinetochore microtubules are also dispensable in meiosis II, although it is technically impossible at the moment to remove even the last traces of kinetochore microtubules, as some microtubules are resistant to canonical drugs [benzimidazole compounds such as MBC carbendazim and TBZ thiabendazole ].
It is also reported that, in mitosis, microtubule-independent nuclear fission also occurs Castagnetti et al. SPBs can separate in the absence of spindle microtubules when cdc11 mutant cells defective in cytokinesis are exposed to microtubule poisons. It is also possible that a constant increase of the nuclear membrane components, which are supposed to be used for nuclear elongation in anaphase, caused an abundance in surplus in the absence of spindle elongation, resulting in aberrant nuclear fission Castagnetti et al.
Interestingly, nuclear fission requires F-actin. This is reminiscent of animal cells in which F-actin-dependent mechanisms promote spindle positioning and orientation [reviewed in Sandquist et al.
The study strikingly showed that chromosome segregation is also fine to some degree. This might be also due to actin-dependent mechanisms as in bacterial cells in which chromosome segregation is driven by actin-like cytoskeleton. It is also possible that the segregation system utilizes any nucleoplasmic factors such as Csi1, as a material that connects mitotic SPBs and kinetochores even in the absence of microtubules, because Csi1 has been shown to connect SPBs and centromeres constantly in interphase Hou et al.
It should be noted that no specific systems have been so far identified that ensure the equal segregation of sister chromatids in eukaryotes besides spindle microtubules. Currently, it is hard to completely rule out the possibility that very tiny residual microtubule seeds remain at SPBs even in the presence of the drug, as such tiny microtubule seeds might be able to connect SPBs and kinetochores clustered altogether at the mitotic onset.
Once such attachments were made, kinetochore-mediated SPB separation might take place similar to the situation in Figure 3C to separate SPBs and segregate sister chromatids.
It has been impossible to completely disrupt microtubules and inhibit regrowth by existing drugs; it would be intriguing to revisit these phenomena again when more effective drugs are invented in the future. The evolutionary origin of meiosis has been discussed from the viewpoint of the phenomena for a long period, and one of the most reasonable ideas must be that meiosis was evolved from mitosis Simchen and Hugerat, Although meiosis is different from mitosis in many ways, one of the most essential characteristics in meiosis could be pairing of homologous chromosomes.
Meiosis might have first evolved from mitosis through the acquisition of homolog pairing as an additional step Wilkins and Holliday, As the molecular mechanisms have been illuminated in the last decades, the idea is getting realistic as evidenced by the genes involved in key events in meiosis. Most of the key events in meiosis appear to be conducted by meiosis-specific genes that are paralogous to those used in mitosis.
Assuming that paralogous genes are generated via gene duplication in the long history of evolution, Spo11 S. The meiotic cohesin Rec8 could likewise be originated from a duplicated copy of the mitotic cohesin Rad Those key factors might have defined the outline of meiosis as a newly acquired division system. In addition to those copied genes, meiosis-specific genes whose ancestors are currently unknown are also created to fine-tune meiotic events to the current state.
On the other hand, we also know that molecules or detailed molecular mechanisms in meiosis have been differentiated depending on species, although the whole system of meiosis per se is common among eukaryotes. The molecular mechanisms are thought to be fine-tuned in each organism depending on internal and external reasons such as the lifestyle and surrounding environment.
Considering similarities and differences among species and in between two types of divisions, we will be able to converge the divergent mechanisms to explore the ultimate origin in the future. MS conceived the framework of the entire manuscript. MS prepared the figures. All the authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
We thank the members of the Masayuki Yamamoto laboratory for the inspiring discussion and support and Yutaka Shirasugi, Naoko Nishizawa, and Rio Fukuchi for their helpful comments.
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Cell , 59— Chromosomes rein back the spindle pole body during horsetail movement in fission yeast meiosis. Save my name and email in this browser for the next time I comment.
Following are the differences between Mitosis and Meiosis: S. Yes, mixing of chromosomes can occur. Reduced by half. Sex cells only: female egg cells or male sperm cells. Do not disappear completely in telophase I. Occurs in Interphase I. The centromeres do not separate during anaphase I, but during anaphase II.
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