Frequencies of mtDNA haplogroups in Southeastern Europe: Croatians, Bosnians and Herzegovinianas, Serbians, Macedonians and Macedonian Romani

Mitochondrial DNA polymorphisms were analyzed in of 1,610 randomly chosen adult men from 11 different regions from southeastern Europe (Croatians, Bosnians and Herzegovinians, Serbians, Macedonians and Macedonian Romani). MtDNA HVS-I region together with RFLP sites diagnostic for main Euroasian and African mtDNA haplogroups were typed to determine haplogroup frequency distribution. The most frequent haplogroup in studied populations was H with the exception of Macedonian Romani among whom the most frequent were South Asian (Indian) specific variants of haplogroup M. The multidimensional scaling plot showed two clusters of populations and two outliers (Macedonian Romani and the most distant from mainland Croatian island of Korčula). The first cluster was formed by populations from three Croatian islands (Hvar, Krk and Brač) and the second cluster was formed by Macedonians, Serbians, Croatians from mainland and coast, Herzegovinians, Bosnians, Slovenians, Poles and Russians. The present analysis does not address a precise evaluation of phylogenetic relations of studied populations although some conclusions about historical migrations could be noticed. More extended conclusions will be possible after deeper phylogenetic and statistical analyses

Frequencies of mtDNA Haplogroups in Southeastern Europe - Croatians, Bosnians and Herzegovinians, Serbians, Macedonians and Macedonian Romani

Mitochondrial DNA polymorphisms were analyzed in of 1,610 randomly chosen adult men from 11 different regions from southeastern Europe (Croatians, Bosnians and Herzegovinians, Serbians, Macedonians and Macedonian Romani). MtDNA HVS-I region together with RFLP sites diagnostic for main Euroasian and African mtDNA haplogroups were typed to determine haplogroup frequency distribution. The most frequent haplogroup in studied populations was H with the exception of Macedonian Romani among whom the most frequent were South Asian (Indian) specific variants of haplogroup M. The multidimensional scaling plot showed two clusters of populations and two outliers (Macedonian Romani and the most distant from mainland Croatian island of Korčula). The first cluster was formed by populations from three Croatian islands (Hvar, Krk and Brač) and the second cluster was formed by Macedonians, Serbians, Croatians from mainland and coast, Herzegovinians, Bosnians, Slovenians, Poles and Russians. The present analysis does not address a precise evaluation of phylogenetic relations of studied populations although some conclusions about historical migrations could be noticed. More extended conclusions will be possible after deeper phylogenetic and statistical analyses

Origin and spread of human mitochondrial DNA haplogroup U7

Human mitochondrial DNA haplogroup U is among the initial maternal founders in Southwest Asia and Europe and one that best indicates matrilineal genetic continuity between late Pleistocene hunter-gatherer groups and present-day populations of Europe. While most haplogroup U subclades are older than 30 thousand years, the comparatively recent coalescence time of the extant variation of haplogroup U7 (~16–19 thousand years ago) suggests that its current distribution is the consequence of more recent dispersal events, despite its wide geographical range across Europe, the Near East and South Asia. Here we report 267 new U7 mitogenomes that – analysed alongside 100 published ones – enable us to discern at least two distinct temporal phases of dispersal, both of which most likely emanated from the Near East. The earlier one began prior to the Holocene (~11.5 thousand years ago) towards South Asia, while the later dispersal took place more recently towards Mediterranean Europe during the Neolithic (~8 thousand years ago). These findings imply that the carriers of haplogroup U7 spread to South Asia and Europe before the suggested Bronze Age expansion of Indo-European languages from the Pontic-Caspian Steppe region

Radiation-induced chromosomal rearrangements in dead Deinococcus radiodurans cells: the role of insertion sequences and RecA protein

U ovom radu istraživani su fundamentalni uzroci stanične smrti u robusnoj bakteriji Deinococcus radiodurans koja preživljava izlaganje ekstremnom isušivanju, ionizirajućem zračenju ili mutagenim kemijskim spojevima. Rezultati ovog istraživanja pokazali su da je ključna „meta“ stanične smrti funkcija (proteom), a ne informacija (genom). Analizirana je sudbina oštećene DNA (dvolančani lomovi i kromosomski rearanžmani u preživjelim i mrtvim stanicama) i oksidacijom oštećenih (karboniliranih) proteina u trenutku "odluke" o preživljenju ili smrti stanice; pronađena je korelacija između stanične smrti i zračenjem izazvane karbonilacije proteina, ali ne i oštećenja molekule DNA. Stanična smrt je inicirana progresivnim gubitkom vitalnih funkcija, uključujući popravak DNA, koji nastaje uslijed povećanja razine ireverzibilnih oštećenja proteina. Dok se popravak DNA odvija slično u ugibajućim i preživjelim stanicama, nepovratna točka smrti je depolarizacija i permeabilnost stanične membrane koja je potaknuta oksidacijom novosintetiziranih membranskih proteina, što u konačnici rezultira fatalnim „otpuštanjem“ staničnih metabolita i iona potrebnih za sve biosintetske procese. Ova fatalna promjena stanične membrane je aktivan proces budući da ovisi o transkripciji i translaciji de novo u letalno ozračenim stanicama bakterije D. radiodurans.This research was focused on the fundamental cause(s) of cell death in a robust bacterium, Deinococcus radiodurans, known to survive extreme exposures to desiccation, radiation or mutagenic chemicals. The results of this study proved that the key target in cell death is function (proteome) rather than information (genome). Analyzing the fate of the damaged DNA (double-strand breaks and chromosomal rearrangements in surviving and dead cells) and oxydatively damaged (carbonylated) proteins when the “decision“ between survival and death takes place, cell death showed correlation with radiation-induced proteome carbonylation but not with DNA breakage. Cell death is initiated by the progressive loss of vital functions, including DNA repair, caused by increasing levels of the irreversible protein damage. While DNA repair proceeds similarly in dying and surviving cells, the deadly point of no-return is membrane depolarization and permeability - triggered by neo-synthesized oxidized membrane proteins - causing the fatal leakage of metabolites and ions required for all biosynthetic processes. This fatal change in cell membrane is an active process since it depends on de novo transcription and translation in lethally irradiated D. radiodurans cells

Radiation-induced chromosomal rearrangements in dead Deinococcus radiodurans cells: the role of insertion sequences and RecA protein

U ovom radu istraživani su fundamentalni uzroci stanične smrti u robusnoj bakteriji Deinococcus radiodurans koja preživljava izlaganje ekstremnom isušivanju, ionizirajućem zračenju ili mutagenim kemijskim spojevima. Rezultati ovog istraživanja pokazali su da je ključna „meta“ stanične smrti funkcija (proteom), a ne informacija (genom). Analizirana je sudbina oštećene DNA (dvolančani lomovi i kromosomski rearanžmani u preživjelim i mrtvim stanicama) i oksidacijom oštećenih (karboniliranih) proteina u trenutku "odluke" o preživljenju ili smrti stanice; pronađena je korelacija između stanične smrti i zračenjem izazvane karbonilacije proteina, ali ne i oštećenja molekule DNA. Stanična smrt je inicirana progresivnim gubitkom vitalnih funkcija, uključujući popravak DNA, koji nastaje uslijed povećanja razine ireverzibilnih oštećenja proteina. Dok se popravak DNA odvija slično u ugibajućim i preživjelim stanicama, nepovratna točka smrti je depolarizacija i permeabilnost stanične membrane koja je potaknuta oksidacijom novosintetiziranih membranskih proteina, što u konačnici rezultira fatalnim „otpuštanjem“ staničnih metabolita i iona potrebnih za sve biosintetske procese. Ova fatalna promjena stanične membrane je aktivan proces budući da ovisi o transkripciji i translaciji de novo u letalno ozračenim stanicama bakterije D. radiodurans.This research was focused on the fundamental cause(s) of cell death in a robust bacterium, Deinococcus radiodurans, known to survive extreme exposures to desiccation, radiation or mutagenic chemicals. The results of this study proved that the key target in cell death is function (proteome) rather than information (genome). Analyzing the fate of the damaged DNA (double-strand breaks and chromosomal rearrangements in surviving and dead cells) and oxydatively damaged (carbonylated) proteins when the “decision“ between survival and death takes place, cell death showed correlation with radiation-induced proteome carbonylation but not with DNA breakage. Cell death is initiated by the progressive loss of vital functions, including DNA repair, caused by increasing levels of the irreversible protein damage. While DNA repair proceeds similarly in dying and surviving cells, the deadly point of no-return is membrane depolarization and permeability - triggered by neo-synthesized oxidized membrane proteins - causing the fatal leakage of metabolites and ions required for all biosynthetic processes. This fatal change in cell membrane is an active process since it depends on de novo transcription and translation in lethally irradiated D. radiodurans cells