Book reviews of:
Hattiesburg: An American City in Black and White By William Sturkey. (Cambridge: Harvard University Press, 2019. Acknowledgements, illustrations, map, notes, index. Pp. 442. 29.95cloth.ISBN978−0−674−97635−1.)ConfederateGeneralsintheTrans−Mississippi,Volume3:EssaysonAmerica’sCivilWar.EditedbyThomasE.SchottandLawrenceLeeHewitt.(Knoxville:UniversityofTennesseePress,2019.Maps,photos,notes,appendix,bibliography,index.Pp.xxiv,374.64.95 cloth. ISBN: 978-1-62190-454-0.)
Mothers of Massive Resistance: White Women and the Politics of White Supremacy. By Elizabeth Gillespie McRae. (New York: Oxford University Press, 2018. Acknowledgements, Abbreviations, illustrations, notes, index. Pp. xiv, 343. 34.95hardcover.ISBN:978−0−19−027171−8.)PollPower:TheVoterEducationProjectandtheMovementfortheBallotintheAmericanSouth.ByEvanFaulkenbury.(ChapelHill:UniversityofNorthCarolinaPress,2019.Acknowledgements,illustrations,notes,index.Pp.xi,200.90 cloth, 27.95paper.ISBN:978−1−4696−5131−6.)LetUsMakeMen:TheTwentiethCenturyBlackPressandaManlyVisionforRacialAdvancement.ByD’WestonHaywood.(ChapelHill:UniversityofNorthCarolinaPress,2018.Acknowledgements,illustrations,map,notes,index.Pp.xi,340.55 cloth, 19.50paper.ISBN:978−1−4696−4338−0.)TheManWhoPunchedJeffersonDavis:ThePoliticalLifeofHenryS.Foote,SouthernUnionist.ByBenWynne.(BatonRouge,LouisianaStateUniversityPress,2018.Acknowledgements,illustrations,notes,index.Pp.ix,323.47.50 cloth. ISBN: 978-0-8071-6933-9.)
Desegregating Dixie: The Catholic Church in the South and Desegregation, 1945-1992. By Mark Newman. (Jackson: University Press of Mississippi, 2018. Acknowledgements, appendices, notes, bibliography, index. Pp. xvii, 455. 90cloth,30 paper. ISBN: 978-1-4968-1886-7.)
The Loyal Republic: Traitors, Slaves, and the Remaking of Citizenship in Civil War America. By Erik Mathisen. (Chapel Hill: The University of North Carolina Press, 2018. Acknowledgments, illustrations, map, notes, index. Pp. xi, 219. 34.95cloth.ISBN:978−1−4696−3632−0.)AberrationofMind:SuicideandSufferingintheCivilWar−EraSouth.ByDianeMillerSommerville.(ChapelHill:UniversityofNorthCarolinaPress,2018.Acknowledgements,notes,bibliography,index.Pp.448.105 cloth, 34.95paper.ISBN:978−1−4696−4330−4.)Women’sWar:FightingandSurvivingtheAmericanCivilWar.ByStephanieMcCurry.(Cambridge,Massachusetts:TheBelknapPressofHarvardUniversityPress,2019.notes,acknowledgements,index.Ppix,297.26.95 hardcover. ISBN: 978-0-674-98797-5.)
Lines Were Drawn: Remembering Court-Ordered Integration at a Mississippi High School. Edited By Teena F. Horn, Alan Huffman, and John G. Jones. (Jackson: University Press of Mississippi, 2016. Acknowledgments, illustrations, map, notes, index. Pp. xi, 266. 35hardback.ISBN:978−1−62846−231−9.)IndustrialDevelopmentandManufacturingintheAntebellumGulfSouth:AReevaluation.ByMichaelS.Frawley.(BatonRouge:LouisianaStateUniversityPress.2019.ix,256pp.Cloth,45.00, ISBN 978-0-8071-7068-7.)
Integration Now: Alexander v. Holmes and the End of Jim Crow Education. By William P. Hustwit. (Chapel Hill: University of North Carolina Press, 2019. 8 halftones, 1 map, notes, bibl., index. 288 pp. $39.95, hardcover. ISBN: 978-1-4696-4855-2.
The catalytic subunit of yeast telomerase, Est2p, is a telomere associated throughout most of the cell cycle, while the Est1p subunit binds only in late S/G2 phase, the time of telomerase action. Est2p binding in G1/early S phase requires a specific interaction between telomerase RNA (TLC1) and Ku80p. Here, we show that in four telomerase-deficient strains (cdc13-2, est1Ä, tlc1-SD, and tlc1-BD), Est2p telomere binding was normal in G1/early S phase but reduced to about 40–50% of wild type levels in late S/G2 phase. Est1p telomere association was low in all four strains. Wild type levels of Est2p telomere binding in late S/G2 phase was Est1p-dependent and required that Est1p be both telomere-bound and associated with a stem-bulge region in TLC1 RNA. In three telomerase-deficient strains in which Est1p is not Est2p-associated (tlc1-SD, tlc1-BD, and est2Ä), Est1p was present at normal levels but its telomere binding was very low. When the G1/early S phase and the late S/G2 phase telomerase recruitment pathways were both disrupted, neither Est2p nor Est1p was telomere-associated. We conclude that reduced levels of Est2p and low Est1p telomere binding in late S/G2 phase correlated with an est phenotype, while a WT level of Est2p binding in G1 was not sufficient to maintain telomeres. In addition, even though Cdc13p and Est1p interact by two hybrid, biochemical and genetic criteria, this interaction did not occur unless Est1p was Est2p-associated, suggesting that Est1p comes to the telomere only as part of the holoenzyme. Finally, the G1 and late S/G2 phase pathways for telomerase recruitment are distinct and are likely the only ones that bring telomerase to telomeres in wild-type cells
Telomere integrity in budding yeast depends on the CST (Cdc13-Stn1-Ten1) and shelterin-like (Rap1-Rif1-Rif2) complexes, which are thought to act independently from each other. Here we show that a specific functional interaction indeed exists among components of the two complexes. In particular, unlike RIF2 deletion, the lack of Rif1 is lethal for stn1ΔC cells and causes a dramatic reduction in viability of cdc13-1 and cdc13-5 mutants. This synthetic interaction between Rif1 and the CST complex occurs independently of rif1Δ-induced alterations in telomere length. Both cdc13-1 rif1Δ and cdc13-5 rif1Δ cells display very high amounts of telomeric single-stranded DNA and DNA damage checkpoint activation, indicating that severe defects in telomere integrity cause their loss of viability. In agreement with this hypothesis, both DNA damage checkpoint activation and lethality in cdc13 rif1Δ cells are partially counteracted by the lack of the Exo1 nuclease, which is involved in telomeric single-stranded DNA generation. The functional interaction between Rif1 and the CST complex is specific, because RIF1 deletion does not enhance checkpoint activation in case of CST-independent telomere capping deficiencies, such as those caused by the absence of Yku or telomerase. Thus, these data highlight a novel role for Rif1 in assisting the essential telomere protection function of the CST complex