| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
Upon commitment to sexual differentiation, fission yeast cells exchange the mating factor signal which induces dramatic remodeling of microtubule architecture to form an astral microtubule array emanating from the spindle pole body (SPB), the yeast centrosome equivalent organelle. During meiotic prophase, an oscillatory nuclear movement termed horsetail nuclear movement (HNM) takes place. HNM is led by the astral microtubule array aided by the dynein-dynactin complex and is proposed to facilitate the alignment of homologous chromosomes necessary for efficient meiotic recombination.
I have identified a meiosis-specific SPB component Hrs1 (also known as Mcp6) and shown that Hrs1 is a key molecule to remodel microtubules into the horsetail-astral array (HAA). Deletion of Hrs1 impaired HAA formation, leading to compromised HNM. Ectopic expression of Hrs1 during the mitotic cell cycle resulted in the formation of a HAA-like astral microtubule array, which drove an oscillatory nuclear movement in interphase cells. Hrs1 interacted with components of the γ-tubulin complex (γ-TuC) as well as with a meiotic SPB component, suggesting that Hrs1 facilitates formation of the HAA, responsible for the vigorous HNM, by stabilizing connection between the SPB and minus ends of microtubules.
Expression of Hrs1 is restricted to meiotic prophase. Upon the onset of meiosis I, Hrs1 abruptly disappeared from SPB even when it was forcibly expressed under the regulation of a strong nmt1 promoter. To see the effect of ectopic Hrs1 expression during meiosis, we isolated a few hrs1 mutants in which mutated Hrs1 proteins were stabilized at the SPB during meiosis I and II. in one of the mutants (hrs1.d10), relative timing of the spindle formation after the cessation of HNM was delayed and malformed spindle were observed. These results indicate a possible mechanism to down-regulate Hrs1 at the onset of meiosis I to ensure a smooth spindle formation.
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