Phenology, Climate, and Adaptation: How Does Dipterocarps Respond to Climate?

Temperature, rainfall and extreme weather have been indicated to affect the phenological patterns and forest productivity by shifting flowering and fruiting seasons and patterns, as well as crop production. Dipterocarpaceae are high value trees for both timber and non-timber forest products. This study aims to determine the response of phenological patterns of flowering and fruiting of Dipterocarps to climate variables. The study was conducted at Way Canguk Research Station of the Bukit Barisan Selatan National Park (BBSNP), Lampung during May-November 2012 by analyzing 14 years (1998-2012) of phenological data of Dipterocarps. The phenology surveys were carried out on monthly basis by estimating the percentage of flowering, fruiting (divided into 0-4 scoring) and the crop production. The results indicated that the phenological patterns of Dipterocarps in the area depicted major and minor patterns without mass-flowering time, different from what have been reported for Kalimantan or North Sumatra. Minor peak flowering season showed regular flowering, particularly during March to July every year. However, there were major flowering seasons in November 2002 (20.2%), September 2006 (21%), and October-November 2011 (20.3%). Average monthly fruit production showed a peak at the end of the dry season. Major flowering season seemed to coincide with the period of major El Nino events in November 2002 and September 2006, while others associated with La Nina. This study suggest that phenology and climate change may have implications in designing strategies for collection of seed materials to support the conservation and plantation programs of the Dipterocarps

Whi2 is a conserved negative regulator of TORC1 in response to low amino acids

International audienceYeast WHI2 was originally identified in a genetic screen for regulators of cell cycle arrest and later suggested to function in general stress responses. However, the function of Whi2 is unknown. Whi2 has predicted structure and sequence similarity to human KCTD family proteins, which have been implicated in several cancers and are causally associated with neurological disorders but are largely uncharacterized. The identification of conserved functions between these yeast and human proteins may provide insight into disease mechanisms. We report that yeast WHI2 is a new negative regulator of TORC1 required to suppress TORC1 activity and cell growth specifically in response to low amino acids. In contrast to current opinion, WHI2 is dispensable for TORC1 inhibition in low glucose. The only widely conserved mechanism that actively suppresses both yeast and mammalian TORC1 specifically in response to low amino acids is the conserved SEACIT/GATOR1 complex that inactivates the TORC1-activating RAG-like GTPases. Unexpectedly, Whi2 acts independently and simultaneously with these established GATOR1-like Npr2-Npr3-Iml1 and RAG-like Gtr1-Gtr2 complexes, and also acts independently of the PKA pathway. Instead, Whi2 inhibits TORC1 activity through its binding partners, protein phosphatases Psr1 and Psr2, which were previously thought to only regulate amino acid levels downstream of TORC1. Furthermore, the ability to suppress TORC1 is conserved in the SKP1/BTB/POZ domain-containing, Whi2-like human protein KCTD11 but not other KCTD family members tested

Whi2 is a conserved negative regulator of TORC1 in response to low amino acids

International audienceYeast WHI2 was originally identified in a genetic screen for regulators of cell cycle arrest and later suggested to function in general stress responses. However, the function of Whi2 is unknown. Whi2 has predicted structure and sequence similarity to human KCTD family proteins, which have been implicated in several cancers and are causally associated with neurological disorders but are largely uncharacterized. The identification of conserved functions between these yeast and human proteins may provide insight into disease mechanisms. We report that yeast WHI2 is a new negative regulator of TORC1 required to suppress TORC1 activity and cell growth specifically in response to low amino acids. In contrast to current opinion, WHI2 is dispensable for TORC1 inhibition in low glucose. The only widely conserved mechanism that actively suppresses both yeast and mammalian TORC1 specifically in response to low amino acids is the conserved SEACIT/GATOR1 complex that inactivates the TORC1-activating RAG-like GTPases. Unexpectedly, Whi2 acts independently and simultaneously with these established GATOR1-like Npr2-Npr3-Iml1 and RAG-like Gtr1-Gtr2 complexes, and also acts independently of the PKA pathway. Instead, Whi2 inhibits TORC1 activity through its binding partners, protein phosphatases Psr1 and Psr2, which were previously thought to only regulate amino acid levels downstream of TORC1. Furthermore, the ability to suppress TORC1 is conserved in the SKP1/BTB/POZ domain-containing, Whi2-like human protein KCTD11 but not other KCTD family members tested