Article

ISSN 0006-2979, Biochemistry (Moscow), 2024, Vol. 89, No. 6, pp. 1014-1023 © The Author(s) 2024. This article is an open access publication.

1014

REVIEW

Activity of DNA Repair Systems

in the Cells of Long-Lived Rodents and Bats

Aleksei A. Popov

, Irina O. Petruseva

, and Olga I. Lavrik

1,2a

Institute of Chemical Biology and Fundamental Medicine, Siberian Branch Russian Academy of Sciences,

630090 Novosibirsk, Russia

Novosibirsk National Research State University, 630090 Novosibirsk, Russia

e-mail: lavrik@niboch.nsc.ru

Received January 24, 2024

Revised March 15, 2024

Accepted April 3, 2024

Abstract— Damages of various origin accumulated in the genomic DNA can lead to the breach of genome sta-

bility, and are considered to be one of the main factors involved in cellular senescence. DNA repair systems in

mammalian cells ensure effective damage removal and repair of the genome structure, therefore, activity of these

systems is expected to be correlated with high maximum lifespan observed in the long-lived mammals. This re-

view discusses current results of the studies focused on determination of the DNA repair system activity and in-

vestigation of the properties of its key regulatory proteins in the cells of long-lived rodents and bats. Based on the

works discussed in the review, it could be concluded that the long-lived rodents and bats in general demonstrate

high efficiency in functioning and regulation of DNA repair systems. Nevertheless, a number of questions around

the study of DNA repair in the cells of long-lived rodents and bats remain poorly understood, answers to which

could open up new avenues for further research.

DOI: 10.1134/S0006297924060038

Keywords: DNA repair, cellular senescence, longevity, poly(ADP-ribose)polymerase1, sirtuin6

Abbreviations: BER, base excision repair; HR,homologous recombination; NER,nucleotide excision repair; NHEJ,non-homol-

ogous DNA end junction; PARP1,poly(ADP-ribose)-polymerase1; SIRT6,sirtuin6 histone deacetylase.

* To whom correspondence should be addressed.

INTRODUCTION

Aging is an age-related deterioration of body phys-

iological functions, which may result in developing car-

diovascular diseases, cancer, and neurodegeneration.

Aging manifests itself at the cellular level as a conse-

quence of pathological changes in cellular homeosta-

sis, accompanied by irreversible cell cycle arrest and

acquisition of a corresponding phenotype by the cell,

development of a chronic inflammatory reaction at the

tissue level, and many other symptoms [1]. Age-related

accumulation of “aging” cells in the body, being depen-

dent on the decreased efficiency of their removal from

tissues, contributes to the body senescence and devel-

opment of the aging-associated diseases [2]. One of the

main causes of the cellular senescence is disruption of

the genome structure. It could occur both spontaneous-

ly (replication errors, deamination of nitrogenous bases

and depurination) and due to exogenous (UV radiation,

drugs, etc.) and endogenous (reactive oxygen species)

factors [3-6]. Various cellular mechanisms are involved

in maintaining the mammalian genome stability [7-9]

and DNA repair systems play an essential role among

them. Many studies have been devoted to correlation

between the DNA repair and aging [5, 10, 11]; decreased

activity of DNA repair systems is known today to lead

to the increased genome damage and damage accumu-

lation rate, which, in turn, results in the significantly

increased risk of the development of pathologies asso-

ciated with aging [9, 12, 13]. At the same time, the re-

sults of comparative studies of the DNA repair system

activity, as well as its function and regulation in the

long-lived mammals have been investigated only to a

small extent. Relevant information on the functional

DNA REPAIR AND LONGEVITY 1015

BIOCHEMISTRY (Moscow) Vol. 89 No. 6 2024

status of DNA repair systems and peculiarities of the

corresponding proteins in the cells of long-lived mam-

mals could provide a more detailed understanding of

the links between the DNA repair and aging.

Various representatives of the Rodentia order are

the most popular models for comparative studies of

aging in mammals [14-16]. There are animals among

them that demonstrate high maximum lifespan (over

30 years), as well as resistance to prolonged exposure

to oxidative stress and cancer [17-19]. Much attention

is also paid to bats (Chiroptera) as a potential model

for studying aging in mammals. On the one hand, it is

due to the high maximum lifespan (about 30-40 years)

observed for many representatives of this order. On the

other hand, it results from a huge lack of knowledge

about the peculiarities of the DNA repair system func-

tioning within bat cells [20]. Hence, search for and in-

vestigation of these peculiarities that promote genome

stability and longevity in the long-lived rodents and

bats could be of great research interest.

Objective of this review is to analyze relevant

data on the activity of DNA repair systems in the cells

of long-lived rodents and bats. In the first part of the

review the described results of the studies devoted to

activity of the DNA repair systems in the cells of these

mammals are presented. In the second part of the re-

view the results of studying activity of the NAD

-depen-

dent poly(ADP-ribose)polymerase 1 (PARP1) and histone

deacetylase sirtuin6 (SIRT6) in the context of investiga-

tion of the considered phylogenetic animal groups are

discussed, since PARP1 and SIRT6 are among the main

regulatory proteins of DNA repair processes. The re-

view overlaps partially with the research of Yamamura

etal. [19], Gorbunova etal. [20] and Boughey etal. [21],

published recently. Information on the results obtained

from the study of DNA repair processes within the cells

of long-lived rodents and bats presented in the review

may be relevant and useful to the researchers focused

not only on the studying molecular basis of longevity

in mammals, including humans, but also on the devel-

oping effective strategy for extension of lifespan and

treatment of aging-associated diseases.

DNA REPAIR SYSTEM ACTIVITY

Specialized DNA repair systems become activat-

ed in the cell in response to DNA damage, and their

functions are associated with the cell cycle regulation

and cell death [22]. Spontaneously formed apurine/apy-

rimidine(AP) sites, single- and double-strand breaks,

DNA–DNA cross-linking, as well as DNA–protein cross-

links and various bulky DNA damages are serious dis-

ruptions of the genome structure, their persistence

could lead to the cells death or their transformation

into the state of cellular senescence. Cells maintain

genome structure, which enables their normal func-

tioning with the help of such efficient DNA repair

systems as base excision repair(BER) and nucleotide

excision repair (NER), as well as homologous recom-

bination(HR) and non-homologous end joining (NHEJ)

ensuring removal of the wide range of damages.

Allthis gives grounds to focus on DNA repair as one of

the main factors promoting longevity [5]. In the search

for interrelations between the maximum lifespan and

efficiency of these DNA repair systems, a number of

experimental works were carried out comparing sta-

tus of the repair systems in the mammalian cells from

organisms with different maximum lifespan: humans,

rodents, and bats.

RNA sequencing (RNA-seq) and subsequent anal-

ysis of expression of the 130 protein genes involved

in DNA repair revealed that expression levels of more

than 30 genes, including genes encoding proteins in-

volved in the BER and NHEJ processes in the liver cells

of naked mole-rat (Heterocephalus glaber, ~28 years)

and humans were considerably higher compared to the

mouse cells (Mus musculus, ~4 years) [23, 24]. There-

sults of qPCR quantitative analysis of the mRNA con-

tent, carried out later, showed that within 24 h after

UV irradiation expression level of many BER and NER

protein genes in the mouse fibroblasts increased sig-

nificantly, while no pronounced response at the expres-

sion level of these genes was shown in the naked mole-

rat cells. At the same time, comparative assessment of

activity of these repair systems showed that the DNA

repair proteins activity in the naked mole-rat is 1.5-3

times higher than in a mouse [25].

Tian et al. [26] showed using the host cell reacti-

vation method (HCR) that there is a significant vari-

ability of the repair efficiency of a plasmid, containing

multiple UV lesions by the NER proteins invivo among

18 rodent species; and there is no correlation between

the plasmid repair efficiency and lifespan. At the same

time, using HCR and another model plasmid, direct cor-

relation was first established between the efficiency of

double-stranded breaks repair by the proteins of NHEJ

systems and HR in the pulmonary (r

 = 0.31; p < 0.05)

and dermal (r

 = 0.57; p < 0.01) fibroblasts and lifespan

within the studied group of rodents [26]. Despite some

disadvantages associated with the difficulty in obtain-

ing model plasmids, advantages of the HCR method

make its further application to be especially in demand

for measuring activity of the DNA repair systems at the

cell level [27].

RNA-seq demonstrated that the cells of the long-

lived Middle East blind mole-rat (Spalax ehrenbergi,

~20years) also revealed higher gene expression levels

of the BER and HR proteins compared to the cells of

the short-lived brown rat (Rattus norvegicus, ~5years)

[28] and mouse [29]. Similar expression levels of

the DNA repair genes in the blind mole-rat and

POPOV et al.1016

BIOCHEMISTRY (Moscow) Vol. 89 No. 6 2024

thenakedmole-rat are believed to be a consequence

of adaptation to hypoxic conditions of their habitat.

Increase in expression of the genes of DNA repair pro-

teins under hypoxic conditions has been also observed

in some other rodents [30, 31].

High resistance of the naked mole-rat cells to

the effects of DNA damaging agents (methyl meth-

anesulfonate, 5-fluorouracil, and etoposide) [32] and

gamma-radiation [33, 34] revealed in the subsequent

studies could be the result of effective functioning

of the DNA repair systems. Dermal fibroblasts of the

long-lived blind mole-rat also show higher resistance

to etoposide compared to the human and mouse cells,

which allows blind mole-rat cells to avoid the stress-

induced aging [35].

Whole genome sequencing (WGS) of the intestinal

and skin cells of 18 mammalian representatives and

subsequent statistical analysis of the results showed

that the mutation accumulation rate in the somatic cell

genome is inversely correlated with the mammalian

lifespan [36]. It is notable that the mutation accumula-

tion rate in the naked mole-rat somatic cells was almost

8-fold lower than that in the mouse cells. In the work

of Robinson etal. [12] the level and rate of the sponta-

neously generated cyclopurine DNA damage accumula-

tion in the wild-type mouse cells and the cells of mice

with reduced ERCC1 expression(NER) were observed.

Using mass spectrometry, it was shown that the con-

tent of cyclopurine in the ERCC1

–/∆

cells of 5-month-old

mice was higher than that in the cells of wild-type mice

of similar age and comparable to the level in the cells

of the older wild-type mice (3 years old). Thus, in the

absence of functionally active NER, accumulation rate

of the spontaneous DNA damage in the cells increases,

and the level of spontaneous damage is approaching

to the values, typical for the aging cells. The results of

β-galactosidase activity analysis in combination with

the data obtained by the FISH method showed that

these damages, if not eliminated, could contribute to

cell senescence in mammalian tissues [12]. These as-

sumptions were experimentally confirmed in the fur-

ther study of mutant mice with ERCC1 gene knockout,

which demonstrated chronic inflammatory reaction

and characteristic aging phenotype [37].

A relatively small number of researches focused

on DNA repair study in bat cells has been conducted;

there have been no studies aimed at determination of

activity of various DNA repair systems. Comparative

transcriptome analysis of the cells from various tis-

sues of the greater mouse-eared bat (Myotis myotis,

~37 years) and other mammals with different lifespan,

such as mice, brown rats, human, and naked mole-rats,

showed that in the greater mouse-eared bat cells ex-

pression level of many genes of the proteins partici-

pating in DNA repair and cell cycle regulation (for ex-

ample, ATM, PARP1, RAD50, RFC3, RPA1, MLH3, XRCC5)

is increased [38]. The later transcriptome analysis of

blood samples of the long-lived greater mouse-eared

bat revealed increased expression level of 32 protein

genes of various DNA repair systems, among which

13genes encode proteins of the NER system [39]. Nota-

bly, gene expression levels of the DNA repair proteins

in the greater mouse-eared bat cells increase with age,

while there is a decrease in the expression level of

these genes in human cells. Using the same methods

and samples, the authors of this work later conduct-

ed comparative transcriptome analysis of the cells ob-

tained from the long-lived greater mouse-eared bat and

the short-lived velvety free-tailed bat (Molossus molos-

sus, ~5.6 years) and showed that expression levels of

the DNA repair protein genes and macroautophagy

protein genes are significantly increased in the cells of

the long-lived greater mouse-eared bat [40].

Based on the presented data, it can be conclud-

ed that the long-lived rodents, unlike the short-lived

ones, do demonstrate high activity of the DNA repair

systems, which contributes to the timely removal of

DNA damages and, as a result, decreased level and rate

of their accumulation in the genome. Taken together,

these data confirm modern ideas about the role of DNA

repair in mammalian aging [5]. However, some contra-

dictions that are observed when comparing the results

of transcriptome analysis and assessing the DNA repair

system activity in rodents [23-25] indicate the need to

conduct experiments aimed at further identification

and study of the proteins participating in this process

by proteomic methods. These experiments should also

be focused on the assessment of activity of the involved

protein, since gene expression levels do not always cor-

relate with the expression levels of the corresponding

proteins, their content in the cell, and especially with

their activity. For the long-lived bats, only increase in

the expression level of the genes encoding DNA repair

proteins has been shown and there is no information

on the functional status of the DNA repair systems in

the cells. Thus, further studies are needed using meth-

ods for determining activity of the DNA repair systems

and quantifying the levels of DNA damage.

PARP1 AND SIRT6,

KEY DNA REPAIR REGULATORS

Effective search for the DNA damages, as well

as assembly of the repair complexes and functioning

of the repair proteins are essentially affected by the

chromatin compaction. In this regard, special atten-

tion is paid to two NAD

-dependent proteins, PARP1

and SIRT6, which play a key role in many cellular

processes, including regulation of repair proteins,

as well as access of those two proteins to chromatin

regions [41, 42].

DNA REPAIR AND LONGEVITY 1017

BIOCHEMISTRY (Moscow) Vol. 89 No. 6 2024

Along with enzymatic functions, PARP1 and SIRT6

act as sensors of DNA damage. PARP1 is able to attract

chromatin remodeling factors and DNA repair proteins

to the damage site, regulating them and its own activi-

ty [43-45] via carrying out poly(ADP-ribosyl)ation reac-

tion with enzymatic activity activation caused by bind-

ing to the DNA damage. There are data revealing that

the p53 protein [46], which plays an important role in

the cell fate determination [47, 48], is involved in the

DNA repair process through interaction with automod-

ified PARP1. Products of the PARP1-mediated synthesis

of branched poly(ADP-ribose) polymers (PAR) are in-

volved in formation of non-membrane structures, so-

called compartments, in which proteins of the repair

complex are concentrated at the damaged DNA region

for effective implementation of this process [49-51].

SIRT6 regulates activity of histones and other proteins

via their deacetylation, which contributes to attraction

of chromatin remodeling factors and binding of the re-

pair proteins to the damaged DNA sites [52, 53]. A num-

ber of studies has shown that SIRT6 is one of the first

to bind the double-stranded DNA breaks, thus facilitat-

ing attraction and mono(ADP-ribosyl)ation of PARP1

[54, 55]. At the same time, there is evidence that PARP1

is the first to bind the double-stranded DNA breaks,

initiating NHEJ or HR processes [56, 57]. In addition to

DNA repair, PARP1 and SIRT6 are actively involved in

the telomere integrity maintenance and cell cycle reg-

ulation [41, 52].

Numerous studies have been conducted exploring

PARP1 and SIRT6, but functioning of these proteins

still needs detailed investigation due to their involve-

ment in a wide variety of cellular processes. Function-

al relationship between PARP1 and SIRT6 with regard

to DNA repair is of great interest, since both proteins

use the same intranuclear NAD

pool to perform their

catalytic functions and, apparently, compete for it [58].

The question of the joint participation of PARP1 and

SIRT6 in the repair of single-strand and double-strand

DNA breaks remains poorly understood; literature data

onthis issue are contradictory [54-57].

With regard to the study of aging, there are also

conflicting experimental data on the role of PARP1

obtained using the PARP1 knockout mice. There is evi-

dence suggesting that PARP1 could be counted among

the factors contributing to aging [59-61] due to its in-

volvement in activation of the transcription factor

NF-κB, since NF-κB stimulates inflammatory response

by expressing proinflammatory cytokines. At the same

time, it was found in the work by Piskunova etal. [62]

that the PARP1 knockout mice, on the contrary, show

signs of accelerated aging. It is noteworthy that SIRT6

contributes to the decrease of NF-κB activation by

deacetylating the H3 histone at the promoter site of the

NF-κB protein gene [63]. Thus, the study of PARP1 and

SIRT6 is a promising research area, the results of which

could, on the one hand, significantly improve our un-

derstanding of the nature of the DNA repair system or-

ganization and regulation in mammalian cells, and, on

the other hand, it could shed light on the role of both

proteins in aging.

Currently, very little work has been done to com-

pare the PARP1 functioning in the mammalian cells

from the species with different lifespans. Grube and

Bürkle [64] performed for the first time comparative

analysis of PARP1 activity in the leukocytes of 13mam-

malian species, which revealed direct correlation (r

= 0.84; p < 0.001) between the activity of this protein and

longevity of the studied animals. Later, these data were

supported by the results of comparing kinetic charac-

teristics of the recombinant human and short-lived

brown rat PARP1 [65, 66]. Recently, it was shown that

the level of PAR production synthesized by PARP1 of

the naked mole-rat cell extract was 1.5-2.5 times higher

than in the extract of mouse cells [25,67]. Photoaffini-

ty modifications of the proteins in the cell extract pro-

duced using photoactive DNAs containing BER interme-

diate analogues demonstrated that the naked mole-rat

PARP1 interacted 2-3 times more efficiently with the

model DNAs than the mouse PARP1. Higher yields of

the photoaffinity modification products of PARP1 in the

cell extract of the naked mole-rat allowed to assume

higher content of this protein [67]. Therefore, compar-

ison of the PARP1 structure and its functioning specifi-

cally in the naked mole-rat with the similar enzyme in

the mouse requires further investigation.

Recently potential role of PARP1 in demethylation

of DNA from mouse embryonic stem cells was analyzed

in the research by Schwarz et al. [68]. Demethylation

and sequential oxidation of 5-methylcytosine to 5-car-

boxycytosine is carried out by the proteins of the TEN

(ten-eleven translocation proteins) complex [69], after

which 5-carboxycytosine is removed by thymine-DNA

glycosylase (TDG) to form an AP site. TDG remains as-

sociated with the AP site and, thereby, restricts access

to it of the BER proteins for some time. Using various

biochemical approaches, PARP1 in the mouse embry-

onic stem cells has been shown to carry out TDG

poly(ADP-ribosyl)ation, promoting its rapid dissocia-

tion from the DNA complex. PARP1 also facilitates both

poly(ADP-ribosyl)ation of itself and of the BER proteins

that is necessary for efficient repair of the AP site

in vitro and in vivo [68]. Taken together, this ensures

not only a faster TDG turnover and, consequently, a

rapid removal of modified bases from DNA, but also

contributes indirectly to the decrease in the DNA meth-

ylation level in the mouse cells. Since the DNA methyl-

ation rate in mammalian blood and skin cells inversely

correlates with maximum lifespan (r

 = 0.81 and 0.80,

respectively; p < 0.001) [70], the results, obtained in

the study by Schwarz etal. [68], support an important

role of PARP1 in regulating BER process and ensuring

POPOV et al.1018

BIOCHEMISTRY (Moscow) Vol. 89 No. 6 2024

Activity of DNA repair systems and its importance for mammalian genome stability. PARP1 (poly(ADP-ribose)-polymerase1) and

SIRT6 (sirtuin6), NAD

-dependent DNA repair regulators.

mammalian longevity. It is worth noting that the level of

available NAD

in the cell is a critically important factor

for the effective PARP1-mediated regulation of BER in

mammalian cells [71]. There is a decrease in the NAD

level and in the DNA repair efficiency in the cells with

age [71, 72]. Further studies revealed another reason

for association between the NAD

concentration and

PARP1 activity in mammalian cells. The PARP1’s part-

ner is DBC1 (deleted breast cancer1 protein), which

blocks its functioning. Protein–protein interactions

between DBC1 and PARP1 are regulated by the NAD

level. Along with the decrease in NAD

level with age,

the DBC1-mediated inhibition of PARP1 activity occurs,

as well as decrease in the DNA repair efficiency [73].

The role of SIRT6 in DNA repair regulation in the

long-lived mammalian cells is being actively investigat-

ed, but still remains poorly understood. Western blot

analysis of the SIRT6 expression in the cells of human

donors with different ages showed an inverse correla-

tion (r

 = 0.65867; p < 0.0001) of the SIRT6 expression

level with the age and direct correlation (r

 = 0.32568;

p < 0.05) with the BER efficacy [74]. Increased SIRT6

expression in the mouse embryonic fibroblasts result-

ed in the almost 2-fold increase of the BER efficacy.

Itis noteworthy that the PARP1 inhibition with PJ34

orknockdown of the corresponding gene in the immor-

talized HCA2-hTERT human adenocarcinoma cells led

to disruption in BER activation regardless of the SIRT6

expression level. According to the authors, it indicates

the need for the SIRT6-mediated PARP1 involvement

toactivate BER [74].

In the work carried out by Tian et al. [26] the

SIRT6 activity was analyzed in rodents with different

lifespan. Direct correlation between the stimulation

DNA REPAIR AND LONGEVITY 1019

BIOCHEMISTRY (Moscow) Vol. 89 No. 6 2024

ofNHEJ (r

 = 0.34; p < 0.05) and HR (r

 = 0.40; p < 0.01)

by high SIRT6 activity and longevity of the studied ro-

dents was established by the HCR method using a cor-

responding plasmid construct. Results of the additional

experiments performed using recombinant SIRT6 of the

long-lived North American beaver (Castor canadensis,

~24 years old) and the short-lived mouse, made it pos-

sible to establish that the SIRT6 of the North American

beaver shows a slightly greater affinity for NAD

and

higher rate of its transformation in the mono(ADP-

ribosyl)ation reactions (K

 = 138.6 ± 10.6 µM and V

max

= 10.4 ± 0.25 rfu/s, respectively), than the mouse SIRT6

 = 150.9 ± 9.6 µM and V

max

 = 5.0 ± 0.1 rfu/s, respective-

ly). It may significantly increase the SIRT6-mediated

stimulation of PARP1 to participate in NHEJ and HR in

the North American beaver cells [26]. The observed dif-

ferences, according to the authors of this work, could

be due to two unique substitutions, His249Gly and

Thr263Cys, found when comparing the SIRT6 amino

acid sequence of the North American beaver with the

mouse protein [26]. Two rare single nucleotide poly-

morphisms identified later in the SIRT6 sequence of

human centenarians, which led to the appearance of

amino acid substitutions of Asn308Lys and Ala313Ser,

were responsible for an almost twofold increase in

the mono(ADP-ribosyl) transferase activity of SIRT6

in the human cells [75].

Despite the fact that there are only few studies of

SIRT6 and PARP1 in the long-lived rodents, the avail-

able results suggest that the tendency to increase activ-

ity of these proteins in the cells of long-lived animals

is caused by the necessity of more effective regulation

of DNA repair processes. The issue of the SIRT6 and

PARP1 functioning and their properties in the cells of

long-lived bats remains completely unexplored. It is

also worth noting that one of the main factors ensur-

ing high efficiency of DNA repair also involves mod-

ulation of SIRT6 and PARP1 activity by other partner

proteins [73, 76, 77]. Considering importance of SIRT6

and PARP1 for the senescence-associated cellular pro-

cesses [61, 63], further study of these proteins is of

great interest.

CONCLUSION

One of the factors ensuring longevity is stability

of the genome structure and functioning. DNA repair

processes play an important role in maintaining ge-

nome stability. The results of the studies considered

in the review allow us to conclude that rodents with

high maximum lifespan demonstrate effective and

well-coordinated functioning of DNA repair systems

(figure). Due to the small amount of available data and,

as a result, insufficient knowledge, the issue of the

functional status of DNA repair systems along with

PARP1 and SIRT6 activity in bats, which demonstrate

high maximum lifespan, is still open today. Overall,

in order to understand high efficiency of the DNA re-

pair systems in the cells of long-lived mammals, it is

necessary to conduct further studies devoted to the

properties of the proteins participating in DNA repair,

as well as their possible contribution to other cellu-

lar processes that may be associated with senescence.

Moreover, direct comparative assessments focused on

the functional status of DNA repair systems in the cells

of long-lived mammals (in addition to the transcrip-

tome analysis of gene expression) using modern ad-

vanced methods should be conducted.

Contributions. I.O.P. and O.I.L. supervised the

study; A.A.P. and I.O.P. prepared the manuscript; O.I.L.

edited the manuscript.

Funding. This work was financially supported

by the Russian Science Foundation (project no.19-74-

10056-P).

Ethics declaration. This work does not describe

any studies involving humans or animals as objects

performed by any of the authors. The authors of this

work declare that they have no conflicts of interest

infinancial or any other sphere.

Open access. This article is licensed under a Cre-

ative Commons Attribution4.0 International License,

which permits use, sharing, adaptation, distribution,

and reproduction in any medium or format, as long

as you give appropriate credit to the original author(s)

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