SAMUDRA Report No. 61, March 2012

Contents: UNCSD: Rio+20. Shrimp Aquaculture in Central America. Sovereign Rights of Indigenous Fishers. Access to Fisheries Information. Harmonizing Fishworkers’ Rights. The Delhi MPA Workshop.

Nutrient Enhanced Coastal Ocean Productivity (NECOP). Data report: CTD and hydrographic data, R/V Pelican cruise, April 3-11, 1993

The Nutrient Enhanced Coastal Ocean Productivity (NECOP) Program is a component of NOAA's Coastal Ocean Program. The central hypothesis of this research is: Anthropogenic nutrient inputs have enhanced coastal ocean productivity with subsequent impacts on coastal ocean water quality, living resource yields, and the global marine carbon cycle. The initial study area for this program is the Mississippi/Atchafalaya River Outflow and adjacent Louisiana shelf region.

On the troll line investigations off Cochin during five fishing seasons. Pt. 1. Investigations during 1960-61 and 1961-62 seasons

There is apparently great scope for improvement of the design and operational aspects of the gear particularly for the effective exploitation of seasonal fisheries like that of seer, tuna, barracuda etc. In order to evolve improved, yet cheap trolling gear regular investigations were undertaken by the Craft & Gear Wing of the Central Institute of Fisheries Technology, off Cochin for five fishing seasons and the results of these studies are incorporated in this paper.

光敏核不育水稻41 kDa和61 kDa蛋白质的发现、N-端序列分析及其雄性不育性状关系的探讨

光敏核不育水稻农垦58S是石明松于1973年在晚粳农垦58的大田中发现的雄性不育突变体，它在长日照下雄性不育可被用于与恢复系杂交生产杂种，而在短日照下雄性可育能用于自交繁殖，它的恢复系来源广泛。基于这些特性，育种学家用光敏核不育水稻建立的二系杂交水稻制种技术有很大的应用潜力。近十几年来，育种学家用农垦58S作基因供体转育了许多新的不育系，研究结果表明育成的粳型不育系均为光敏不育系，但在育成的籼型不育系中，绝大多数丧失光敏核不育特性，变成温敏不育系。目前因不知光敏核不育的分子遗传机制，尚不能解释这些问题。 本文用双向电泳技术分析了农垦58S和农垦58苗期和育性转换光敏感期叶绿体蛋白质的差异，在农垦58S中发现三个蛋白质(Pl，P2和P3)，其中Pl和P2在苗期和光敏感期叶片内均存在，P3仅在光敏感期的叶片中存在，它们不受长日照或短日照处理的影响。农垦58没有这三个蛋白质。 用制备型双向电泳纯化后，得到SDS - PAGE和IEF纯的Pl和P2。经SDS-PAGE和IEF测定，Pl的等电点是6.2，分子量是41 kDa;P2的等电点是5.8，分子量是61 kDa。现称Pl为P41，P2为P61。氨基酸序列分析和同源性检索发现P41与水稻叶绿体ATP合成酶p亚基和酵母转录因子CAD1有同源性，此外，P41的N-端序列中有一个与蛋白激酶催化核心中的多功能motif Y-G-X-G-X- (P/T)-G-V相似的序列;P61的14个氨基酸长的N-端序列与水稻叶绿体ATP合成酶β亚基的一致。P41和P61 N-端前12个氨基酸的序列也完全一致。 PCR扩增和Southern杂交分析没有发现农垦58S和农垦58之间ATP合成酶β亚基基因(atpB)的多态性。Nothern杂交分析表明农垦58S中仅有一种、与农垦58 atpB mRNA分子量相同的atpB转录产物，但它的atpB mRNA丰度明显低于农垦58的。没有检测到突变的atpB和其它形式的atpB转录产物。 分析P41和P61在其它水稻材料中的分布特点发现它们在粳型光敏不育系7001S、5088S、31301S、C407S和1647S，籼型光敏不育系W7415S和W9451S以及温（光）敏不育系培矮64S中存在，而在对照材料三系水稻马协A、珍汕97A、马协B、珍汕97B和明恢63以及常规粳稻C94153中不存在。根据这些不育系的系谱和它们与农垦58S之间基因的等位性研究结果，讨论了P41和P61与光敏核不育性的可能联系。

Yeast screens identify the RNA polymerase II CTD and SPT5 as relevant targets of BRCA1 interaction.

BRCA1 has been implicated in numerous DNA repair pathways that maintain genome integrity, however the function responsible for its tumor suppressor activity in breast cancer remains obscure. To identify the most highly conserved of the many BRCA1 functions, we screened the evolutionarily distant eukaryote Saccharomyces cerevisiae for mutants that suppressed the G1 checkpoint arrest and lethality induced following heterologous BRCA1 expression. A genome-wide screen in the diploid deletion collection combined with a screen of ionizing radiation sensitive gene deletions identified mutants that permit growth in the presence of BRCA1. These genes delineate a metabolic mRNA pathway that temporally links transcription elongation (SPT4, SPT5, CTK1, DEF1) to nucleopore-mediated mRNA export (ASM4, MLP1, MLP2, NUP2, NUP53, NUP120, NUP133, NUP170, NUP188, POM34) and cytoplasmic mRNA decay at P-bodies (CCR4, DHH1). Strikingly, BRCA1 interacted with the phosphorylated RNA polymerase II (RNAPII) carboxy terminal domain (P-CTD), phosphorylated in the pattern specified by the CTDK-I kinase, to induce DEF1-dependent cleavage and accumulation of a RNAPII fragment containing the P-CTD. Significantly, breast cancer associated BRCT domain defects in BRCA1 that suppressed P-CTD cleavage and lethality in yeast also suppressed the physical interaction of BRCA1 with human SPT5 in breast epithelial cells, thus confirming SPT5 as a relevant target of BRCA1 interaction. Furthermore, enhanced P-CTD cleavage was observed in both yeast and human breast cells following UV-irradiation indicating a conserved eukaryotic damage response. Moreover, P-CTD cleavage in breast epithelial cells was BRCA1-dependent since damage-induced P-CTD cleavage was only observed in the mutant BRCA1 cell line HCC1937 following ectopic expression of wild type BRCA1. Finally, BRCA1, SPT5 and hyperphosphorylated RPB1 form a complex that was rapidly degraded following MMS treatment in wild type but not BRCA1 mutant breast cells. These results extend the mechanistic links between BRCA1 and transcriptional consequences in response to DNA damage and suggest an important role for RNAPII P-CTD cleavage in BRCA1-mediated cancer suppression.