Mad3 modulates the G ₁ Cdk and acts as a timer in the Start network

Abstract

Cells maintain their size within limits over successive generations to maximize fitness and survival. Sizer, timer, and adder behaviors have been proposed as possible alternatives to coordinate growth and cell cycle progression. Regarding budding yeast cells, a sizer mechanism is thought to rule cell cycle entry at Start. However, while many proteins controlling the size of these cells have been identified, the mechanistic framework in which they participate to achieve cell size homeostasis is not understood. We show here that intertwined APC and SCF degradation machineries with specific adaptor proteins drive cyclic accumulation of the G 1 Cdk in the nucleus, reaching maximal levels at Start. The mechanism incorporates Mad3, a centromeric-signaling protein that subordinates G 1 progression to the previous mitosis as a memory factor. This alternating-degradation device displays the properties of a timer and, together with the sizer device, would constitute a key determinant of cell cycle entry.

Actively tunable weak and strong couplings in epsilon-near-zero ultrathin film-based Weyl semimetallic photonic crystals

“…Owing to the mature thin-film technologies and associated applications, layered stacks that support polaritons have attracted much attention in the manipulation of light waves [1][2][3][4][5]. Bloch surface waves (BSWs) are electromagnetic (EM) waves exist at the interface of a truncated periodic * Authors to whom any correspondence should be addressed.…”