Kyushu University · 생화학·유전·분자생물학
요하 이와사 교수의 연구실은 진화 생물학과 생물학적 시스템의 동적 거동을 수학적 모델링을 통해 연구합니다. 주요 연구 분야로는 암의 유전자적 진화, 성적 선택 이론에서의 '손해 원리'(handicap principle), 그리고 생물 종의 생존 전략과 자원 배분 전략의 최적화가 포함됩니다. 특히, 유전적 변이, 돌연변이 압력, 세포 집단 내의 확률적 진화 과정을 수학적으로 분석함으로써 생물 현상의 근본 원리를 밝혀내는 데 초점을 맞추고 있습니다. 이는 암 치료 내성, 생태계 내 상호작용, 생물의 생식 전략 등 실제 생물학적 문제에도 응용됩니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
We use a general additive quantitative genetic model to study the evolution of costly female mate choice by the "handicap" principle. Two necessary conditions must be satisfied for costly preference to evolve. The conditions are (i) biased mutation pressure on viability and (ii) a direct relationship between the degree of expression of the male mating character and viability. These two conditions explain the success and failure of previous models of the "handicap" principle. Our model also appli
The optimal-patch-use problem in predation theory is investigated by use of a stochastic discrete model to match experimental situations when deterministic continuous models are inappropriate. We first consider three elementary strategies, differing in when to leave the patch in which the predator has been foraging; namely, (1) a fixed time has passed, (2) a fixed number of prey has been captured, and (3) the interval between two successive catches has exceeded a fixed time. Each of these fixed
Males of many species use multiple sexual ornaments in their courtship display. We investigate the evolution of female sexual preferences for more than a single male trait by the handicap process. The handicap process assumes that ornaments are indicators of male quality, and a female benefits from mate choice by her offspring inheriting "good genes" that increase survival chances. A new handicap model is developed that allows equilibria to be given in terms of selection pressures, independent o
We study a situation that arises in the somatic evolution of cancer. Consider a finite population of replicating cells and a sequence of mutations: type 0 can mutate to type 1, which can mutate to type 2. There is no back mutation. We start with a homogeneous population of type 0. Mutants of type 1 emerge and either become extinct or reach fixation. In both cases, they can generate type 2, which also can become extinct or reach fixation. If mutation rates are small compared to the inverse of the
Acquired drug resistance is a major limitation for cancer therapy. Often, one genetic alteration suffices to confer resistance to an otherwise successful therapy. However, little is known about the dynamics of the emergence of resistant tumor cells. In this article, we consider an exponentially growing population starting from one cancer cell that is sensitive to therapy. Sensitive cancer cells can mutate into resistant ones, which have relative fitness alpha prior to therapy. In the special cas
The optimal growth schedule of a deciduous perennial plant is studied theoretically. We make three basic assumptions. First, the daily net photosynthetic rate of a plant increases but saturates with the size of the production part (vegetative organs working for photosynthesis). Second, the production part is discarded at the end of a growing season, but it may be rebuilt at the beginning of the next season using stored material. And finally, the plant maximizes the lifetime reproductive investme
Many zooplankters in lakes and oceans assemble in the upper waters at night and sink to the lower layers in the day. Planktivores also migrate following zooplankters. This diel migration is studied by analyzing a habitat selection game between predators and prey, based on the predation hypothesis, i.e., in the daytime zooplankton avoid predators (fish) that hunt by sight at the cost of reduced grazing on phytoplankton. The equilibrium distribution of the game is as follows. When the efficiency o