Parental Age Affects Somatic Mutation Rates in the Progeny of Flowering Plants

In humans, it is well known that the parental reproductive age has a strong influence on mutations transmitted to their progeny. Meiotic nondisjunction is known to increase in older mothers, and base substitutions tend to go up with paternal reproductive age. Hence, it is clear that the germinal mutation rates are a function of both maternal and paternal ages in humans. In contrast, it is unknown whether the parental reproductive age has an effect on somatic mutation rates in the progeny, because these are rare and difficult to detect. To address this question, we took advantage of the plant model system Arabidopsis (Arabidopsis thaliana), where mutation detector lines allow for an easy quantitation of somatic mutations, to test the effect of parental age on somatic mutation rates in the progeny. Although we found no significant effect of parental age on base substitutions, we found that frameshift mutations and transposition events increased in the progeny of older parents, an effect that is stronger through the maternal line. In contrast, intrachromosomal recombination events in the progeny decrease with the age of the parents in a parent-of-origin-dependent manner. Our results clearly show that parental reproductive age affects somatic mutation rates in the progeny and, thus, that some form of age-dependent information, which affects the frequency of double-strand breaks and possibly other processes involved in maintaining genome integrity, is transmitted through the gametes.In humans, it has long been recognized that the reproductive age of the parents has an influence on the health of their progeny. An older reproductive age of the mother is known to increase the fraction of aneuploid gamete formation (Hurles, 2012). For instance, the risk for a trisomy increases from 2% to 3% for mothers in their 20s to more than 30% for mothers in their 40s (Hassold and Hunt, 2009). The age of the father also has an effect on the frequency of spontaneous congenital disorders and common complex diseases, such as autism and some cancers (Goriely and Wilkie, 2012). Indeed, sperm from 36- to 57-year-old men have more double-strand breaks (DSBs) than those of 20- to 35-year-old individuals (Singh et al., 2003). Similarly, the efficiency of DSB repair was reported to decrease with age in vegetative tissues of the plant model system Arabidopsis (Arabidopsis thaliana; Boyko et al., 2006).Owing to the continuous divisions of spermatogonial stem cells, the male germline of humans is thought to be more mutagenic than the female germline. Indeed, it was shown that the paternal germline is more mutagenic than the maternal one with respect to base substitutions (Kong et al., 2012) and replication slippage errors at microsatellites (Sun et al., 2012). It is also known that carriers of germline mutations in mismatch repair (MMR) genes in humans are prone to get colorectal cancer and that the risk depends on the parent-of-origin of the mutation (van Vliet et al., 2011). The molecular basis of these parental effects is not entirely clear but is likely to involve higher rates of nondisjunction during female meiosis, higher mutation rates during spermatogenesis, and probably additional effects of aging.In contrast to the effect of parental age on germline mutations, not much is known about potential effects of parental reproductive age on somatic mutation rates in the offspring. However, it has been shown in animal studies that radiation of males can lead to somatic mutations in their progeny—and subsequent generations—that cannot be attributed to mutations in the paternal germline (for review, see Little et al., 2013). Moreover, several recent studies have illustrated the existence of complex parental and transgenerational effects in humans, although their molecular basis is not clear (Grossniklaus et al., 2013). These effects can be of either genetic nature (but the effect is seen even in offspring that did not inherit the genetic variant from their parents; for review, see Nadeau, 2009) or epigenetic nature (where environmental influences can possibly exert effects on subsequent generations; for review, see Pembrey et al., 2006; Pembrey, 2010; Curley et al., 2011). It is currently not known whether such parental effects affect the somatic mutation rates in the offspring or whether the effects are modulated by parental age.Taking advantage of the plant model system Arabidopsis, in which various somatic mutation rates can readily be assessed (Bashir et al., 2014), we investigated the effects of parental reproductive age on somatic mutation rates in the progeny. We report that there is a pronounced effect of parental age on somatic mutation rates in their offspring in a parent-of-origin-dependent fashion. Thus, some form of parental information, which is inherited through the gametes to the next generation, seems to alter the somatic mutation rates in the progeny and changes with parental reproductive age.     

Ethics in Science

Ethics are a set of moral principles and values a civilized society follows. Doing science with principles of ethics is the bedrock of scientific activity. The society trusts that the results and the projected outcome of any scientific activity is based on an honest and conscientious attempt by the scientific community. However, during the last few decades, there has been an explosion of knowledge and the advent of digital age. We can access the publications of competitors with just a “click”. The evaluation parameters have evolved a lot and are based on impact factors, h-index and citations. There is a general feeling that the scientific community is under a lot of pressure for fulfilling the criteria for upward growth and even retention of the positions held. The noble profession of scientific research and academics has been marred by the temptation to falsify and fabricate data, plagiarism and other unethical practices. Broadly speaking, the breach of ethics involves: plagiarism, falsification of data, redundant (duplicate) publication, drawing far-fetched conclusions without hard data, for early publicity, gift authorship (receiving as well as giving), not giving sufficient attention and consideration to scholars and post-docs as per the norms, self promotion at the cost of team-members, treating colleagues (overall all juniors) in a feudal way and Machiavellianism (cunningness and duplicity in general conduct and push to positions of power and pelf). Misconduct in Indian academics and science is also under a lot of focus. It is important and urgent that science, engineering, and health departments and institutions in our country have in place systems for education and training in pursuit of science with ethics by sound and professional courses in Responsible Conduct of Research. All research and academic institution must have the Office of Ethics for information, guidelines, training and professional oversight of conduct of research with the ethos and ethics of research.     

Analysis of length‐weight relationship of sympatric hill stream teleosts Barilius bendelisis (Hamilton, 1807) and Barilius vagra (Hamilton, 1822) from Garhwal Himalaya,India

The present study describes the length–weight relationships (LWRs) of two important ornamental hill stream fishes, Barilius bendelisis and Barilius vagra (Hamilton), of northern India. A total of 630 specimens were collected from January to June 2011 in a spring‐fed stream in Garhwal Himalaya, India. Information regarding LWRs of these species was not yet available in FishBase.     

Length–weight relationship of two fish species from Poonch River,Western Indian Himalaya: Glyptothorax kashmirensis (Hora, 1923) and Crossocheilus diplochilus (Heckel, 1838)

This study provides the first report of length–weight relationships (LWRs) for two fish species, Glyptothorax kashmirensis and Crossocheilus diplochilus, collected from the Poonch River, one of the lesser tributaries to the Indus basin in India. New maximum length records are reported for both species.     

Adenine versus guanine DNA adducts of aristolochic acids: role of the carcinogen–purine linkage in the differential global genomic repair propensity

Computational modeling is employed to provide a plausible structural explanation for the experimentally-observed differential global genome repair (GGR) propensity of the ALII-N²-dG and ALII-N⁶-dA DNA adducts of aristolochic acid II. Our modeling studies suggest that an intrinsic twist at the carcinogen–purine linkage of ALII-N²-dG induces lesion site structural perturbations and conformational heterogeneity of damaged DNA. These structural characteristics correlate with the relative repair propensities of AA-adducts, where GGR recognition occurs for ALII-N²-dG, but is evaded for intrinsically planar ALII-N⁶-dA that minimally distorts DNA and restricts the conformational flexibility of the damaged duplex. The present analysis on the ALII adduct model systems will inspire future experimental studies on these adducts, and thereby may extend the list of structural factors that directly correlate with the propensity for GGR recognition.