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. 2015 Jul 30;10(7):e0134297. doi: 10.1371/journal.pone.0134297

Fig 5. Model: Tel1/Mec1 phosphorylation of Hop1 at the T318 and S298 ensures effective coupling of meiotic recombination and progression.

Fig 5

(i) Spo11-catalysis of meiotic DSBs triggers Tel1/Mec1 phosphorylation of chromosome bound Hop1 at multiple residues, including the T318 and S298. (ii) The phospho-T318 mediates the initial Mek1-recruitment and phosphorylation, independently of the phospho-S298. (iii) The phospho-S298 promotes stable Hop1-Mek1 interaction on chromosomes. (iv) The phospho-T318 and phospho-S298 promote spore viability by ensuring inter-homolog repair of meiotic breaks; available genetic evidence suggests that the phospho-T318 and phospho-S298 might be involved in regulating the Dmc1- and Rad51-dependent repair process, respectively (see text). (v) Once the essential crossover requirement is met, Ndt80 is activated, leading to exit from meiotic prophase (vi) and irreversible inactivation of Spo11-complex (vi). (viii) Hop1/Mek1 de-phosphorylation and removal from chromosomes ensue, accounting for the transient activation of the Hop1/Mek1-signalling during unchallenged meiosis. (ix, x) During challenged meiosis (e.g. dmc1Δ), Mek1 undergoes the Hop1 phospho-S298-dependent hyper-phosphorylation (ix), necessary for implementing a meiotic checkpoint response (x).